Thomee - Patellofemoral Pain Syndrome

REVIEW ARTICLE
Sports Med 1999 Oct; 28 (4): 245-262

0112-1642/99/0010-0245/$09.00/0
Adis International Limited. All rights reserved.
Patellofemoral Pain Syndrome

A Review of Current Issues
Roland Thome,1 Jesper Augustsson1 and Jon Karlsson2
1 Muscle Laboratory, Department of Rehabilitation Medicine, Sahlgrenska University Hospital,
Gteborg, Sweden
2 Department of Orthopaedics, Sahlgrenska University Hospital, Gteborg, Sweden
Contents
Abstract
. . . . . . . . . . . . . . . . . . . . . . . .
1. Definition of Patellofemoral Pain Syndrome (PFPS)
2. The Patellofemoral Joint . . . . . . . . . . . . . . . .
2.1 Anatomy and Biomechanics . . . . . . . . . .
2.2 Cartilage Properties . . . . . . . . . . . . . . .
3. Incidence of PFPS . . . . . . . . . . . . . . . . . . .
4. Aetiology of PFPS . . . . . . . . . . . . . . . . . . . .
4.1 Malalignment . . . . . . . . . . . . . . . . . . .
4.2 Muscular Imbalance . . . . . . . . . . . . . . .
4.3 Overactivity . . . . . . . . . . . . . . . . . . . .
5. Symptoms . . . . . . . . . . . . . . . . . . . . . . . .
5.1 Pain . . . . . . . . . . . . . . . . . . . . . . . .
6. Treatment . . . . . . . . . . . . . . . . . . . . . . . .
6.1 Patellar Taping . . . . . . . . . . . . . . . . . .
6.2 Surgical Treatment . . . . . . . . . . . . . . . .
7. Conclusion . . . . . . . . . . . . . . . . . . . . . . .
Abstract
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245
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There is no clear consensus in the literature concerning the terminology, aetiology and treatment for pain in the anterior part of the knee. The term anterior
knee pain is suggested to encompass all pain-related problems. By excluding
anterior knee pain due to intra-articular pathology, peripatellar tendinitis or bursitis,
plica syndromes, Sinding Larsens disease, Osgood Schlatters disease, neuromas
and other rarely occurring pathologies, it is suggested that remaining patients
with a clinical presentation of anterior knee pain could be diagnosed with patellofemoral pain syndrome (PFPS). Three major contributing factors of PFPS are
discussed: (i) malalignment of the lower extremity and/or the patella; (ii) muscular imbalance of the lower extremity; and (iii) overactivity.
The significance of lower extremity alignment factors and pathological limits
needs further investigation. It is possible that the definitions used for malalignment should be re-evaluated, as the scientific support is very weak for determining
when alignment is normal and when there is malalignment. Consequently, pathological limits must be clarified, along with evaluation of risk factors for acquiring
PFPS.
Muscle tightness and muscular imbalance of the lower extremity muscles with
246
Thome et al.
decreased strength due to hypotrophy or inhibition have been suggested, but

remain unclear as potential causes of PFPS. Decreased knee extensor strength is
a common finding in patients with PFPS. Various patterns of weaknesses have
been reported, with selective weakness in eccentric muscle strength, within the
quadriceps muscle and in terminal knee extension. The significance of muscle
function in a closed versus open kinetic chain has been discussed, but is far from
well investigated. It is clear that further studies are necessary in order to establish
the significance of various strength deficits and muscular imbalances, and to
clarify whether a specific disturbance in muscular activation is a cause or an effect
(or both) of PFPS.
The most common symptoms in patients with PFPS are pain during and after
physical activity, during bodyweight loading of the lower extremities in walking
up/down stairs and squatting, and in sitting with the knees flexed. However, the
source of patellofemoral pain in patients with PFPS cannot be sufficiently explained. There are several types of clinical manifestation of pain, and therefore a
differentiated documentation of the patients pain symptoms is necessary. The
connection between strength, pain and inhibition, as well as between personality
and pain, needs further investigation.
Many different treatment protocols are described in the literature and recent
studies advocate a comprehensive treatment approach allowing for an individual
and specifically designed treatment. Surgical treatment is rarely indicated.
It is strongly suggested that, when presenting studies on PFPS, a detailed
description should be provided of the diagnosis, inclusion and exclusion criteria
of the patients should be specified along with a detailed methodology, and the
conclusions drawn should be compared with those of other studies in the published
literature. As this is not the case in most studies on PFPS found in the literature,
it is only possible to make general comparisons. In order to further develop treatment models for PFPS we advocate prospective, randomised, controlled, long
term studies using validated outcome measures. However, there is a strong need
for basic research on the nature and aetiology of PFPS in order to better understand this mysterious syndrome.
1. Definition of Patellofemoral Pain

Syndrome (PFPS)
There is no clear consensus in the literature on
the terminology for pain in the anterior part of the
knee.[1] Patellofemoral pain syndrome (PFPS) is
difficult to define, as patients experience a variety
of symptoms from the patellofemoral joint with different levels of pain and physical impairment. The
terminology is thus still widely discussed. Anterior
knee pain, chondromalacia patella, patellofemoral
arthralgia, patellar pain, patellar pain syndrome and
patellofemoral pain are often used synonymously
with PFPS.[2,3]
The term anterior knee pain is suggested to

encompass all pain-related problems of the anterior
part of the knee.[3-5] By excluding anterior knee
pain due to intra-articular pathology, peripatellar
tendinitis or bursitis (table I), plica syndromes,
Sinding Larsens disease, Osgood Schlatters disease, neuromas and other rarely occurring pathologies it is suggested that remaining patients with a
clinical presentation of anterior knee pain could be
diagnosed with PFPS.[3,5] The term patellofemoral
seems appropriate, as no distinction can be made
as to which specific structure of the patella or the
femur is affected. Pain is the symptom that all
patients experience, but patients have other sympSports Med 1999 Oct; 28 (4)
247
Table I. Pathologies that can generate anterior knee pain

Intra-articular pathology (including both the tibiofemoral and patellofemoral joint)
Peripatellar tendinitis or bursitis
Cartilage damage
Quadriceps tendinitis
Menisci, ligament and capsular damage
Patellar tendinitis
Sequelae after patellar fracture, dislocation or subluxation
Iliotibial band friction syndrome
Sequelae after knee surgery
Pre- and infrapatellar bursitis

Pes anserinus bursitis
toms as well, and thus it is appropriate to use the

word syndrome, defined as a group of signs and
symptoms that occur together and characterise a
particular abnormality.[6]
The term chondromalacia patellae, defined at
the beginning of the 20th century to describe pathological changes of the retropatellar cartilage,[7,8] was
for half a century, used as a synonym for the syndrome of patellofemoral pain. However, several
studies during the last 2 decades have shown a poor
correlation between articular cartilage damage and
the still not well-defined pain mechanism of retropatellar pain.[4,9-15]
2. The Patellofemoral Joint
2.1 Anatomy and Biomechanics
The patellofemoral joint consists of the patella,

the distal and anterior parts of the femur, articular
surfaces and surrounding supporting structures. The
patella is a sesamoid bone of relatively constant
length, width and thickness. Seventy-five percent
of the posterior surface of the patella is covered by
cartilage up to 5mm thick, making it the thickest in
the body. The patella increases the lever arm for
the quadriceps/patellar tendon by up to 50% and
also protects the anterior part of the knee joint (fig.
1).[2,16-18]
The patella is passively stabilised by the shape
of the patella, the trochlea of the femur and the
peripatellar retinaculum. The dynamic stabilisers
of the patella include the pes anserinus and semimembranosus muscles, rotating the tibia inward,
the biceps femoris muscle, rotating the tibia outward, the vastus medialis muscle, pulling the patella medially, the vastus lateralis (VL) muscle,
pulling laterally, and the vastus intermedius and
rectus femoris muscles, pulling proximally/laterally. The distal part of the vastus medialis, the vastus medialis obliquus (VMO) muscle, has its own
nerve supply and can pull the patella medially at a
knee angle of 65 (fig. 1).[2,16,17,20]
During extension from approximately 30 of
knee flexion, the tibia rotates outwards and the patella is guided through the trochlea of the femur by
the interacting heads of the quadriceps muscle. At
full knee extension, the patella rests on the suprapatellar fatpad/bursa. During knee flexion from full
knee extension, the distal part of the patella comes
in contact with the lateral femoral condyle at 10 to
20 of knee flexion, and the patella then follows an
S-shaped curve through the trochlea. The part of
the patellar surface articulating with the femur moves
proximally during flexion of the knee (fig. 1).[2,16-18]
Patellofemoral compression forces increase with
increasing knee angles up to 90 of knee flexion
and can reach up to 8 times bodyweight.[2]
2.2 Cartilage Properties
The cartilage has viscous and elastic properties,

i.e. a fluid component for force absorption and lubrication of the articular surface, and elasticity to
distribute and absorb forces. The cartilage, supported
by subchondral bone, is divided into 3 main layers.
The basal layer attaching to the subchondral bone,
with a perpendicular collagen orientation, is highly
efficient for force transfer and absorption. The second layer of collagen bundles is efficient in resisting shear and has high shock-absorbing qualities
owing to the high viscosity. The surface layer has
tangential-orientated collagen with very low friction, which facilitates motion (fig. 2). Nutrition to
the cartilage is supplied through diffusion from the
synovial fluid. Pressure changes the permeability
Sports Med 1999 Oct; 28 (4)
248
Thome et al.
Anterior superior
iliac spine
Q angle
Vastus
lateralis
30-40
Vastus
medialis
50
65
Vastus
medialis
obliquus
Centre of
patella
Tibial
tuberosity
90
45
Lateral
20
Medial
Among 15 year olds, the incidence was 10%. The

major symptoms were pain and crepitation in the
patellofemoral joint, especially during loading of
this joint and palpation of the patella. In addition,
pain while sitting and occasional weakness and
catching sensations were reported. The symptoms
often prohibited the students from participating in
school physical education, and recreational and
competitive sports. Fairbank et al.[23] studied 446
randomly-selected students aged 13 to 19 years.
The symptomatology was the same as in the study
by Hrding.[24] During the year prior to the study,
136 students (30%) had experienced anterior knee
pain. Of these 136 students, 25 had stopped participating in sports. No difference was found between
students with knee pain and those without, in terms
of joint mobility, Q angle, genu valgum and anteversion of the femoral neck.
4. Aetiology of PFPS
135
Fig. 1. The articular surfaces of the patellofemoral joint and patella. The Q angle and the angles of pull by the different parts
of the quadriceps muscle are illustrated on the left. Shaded
areas on the right indicate areas of articular contact on the patella with increasing knee flexion.[16-19]
of the cartilage, and synovial fluid diffuses into the

middle layer. A lubricating fluid is pressed out to
the articular surface, resulting in a nearly frictionless surface (fig. 2).[2,16,17]
3. Incidence of PFPS
Among injuries to physically active adolescents
and young adults, knee problems are one of the
most common, of which anterior knee pain is the
most frequent complaint. In reports from different
sports medicine clinics, knee problems account for
23 to 31% of injuries and complaints, where pain
conditions related to the patellofemoral joint are
the most common.[2,11,21-28] Hrding[24] reported that,
among 1990 students between the ages of 10 and
19 years, anterior knee pain was the most frequent
complaint and was seen in 3.3% of this group.
To assess the degree of PFPS, a variety of symptoms and different levels of pain and physical impairment must be considered. The aetiology is still
unclear in many patients. Three major contributing
factors increasing the risk of developing PFPS are
discussed: malalignment of the lower extremity
and/or the patella, muscular imbalance of the lower
extremity, and overactivity.[2-4,16,29,30]
4.1 Malalignment
4.1.1 Malalignment of the Lower Extremity
Malalignment of the lower extremity has been

considered a contributory factor in the development
of PFPS. Lower extremity alignment factors associated with patients with PFPS include femoral neck
anteversion, genu valgum, knee hyperextension, Q
angle, tibia varum and excessive rearfoot pronation.[2,31] However, clinical studies have not been
able to demonstrate biomechanical or alignment differences between patients with PFPS and healthy
individuals.[3,5,23,32,33] Fulkerson and Hungerford (in
Grayson[2]) did not find any direct correlation between a high Q angle and patellofemoral pain, an
opinion supported by others.[3,23,32-34] A high Q angle
may be a contributing factor in maintaining PFPS
once it has been acquired, but this is not very well

studied. However, Messier et al.[35] studied 36 male
and female runners between 16 and 50 years of age
and found that the Q angle was a discriminator between runners with PFPS and symptom-free runners.
Reid[3] questioned the use of the term malalignment and argued that 60 to 80% of the normal population falls into a category generally classified as
malalignment.
4.1.2 Patellar Malalignment
The shape of the patellar and femoral surfaces,

the configuration of the trochlea and the inter-relationship between these factors are often discussed. Three different patterns of patellar
malalignment have been described in the literature:
subluxation without tilting, subluxation with tilting, and tilting without subluxation.[36,37] However, no difference was found with computerised
tomography (CT) between the patients most
symptomatic and least symptomatic knees in a
study by Thome et al.,[5] and the values for patellar tilt angle, congruence angle and patellar subluxation were found to be within normal limits.[37-39]
These results are in contrast with those of Insall et
al.,[40] using radiographic examination, who stated
that patellar tracking abnormalities were the major
cause of patellar pain. The reason for the normal
CT values in the study by Thome et al.[5] was
probably that the patients had patellofemoral pain
only and no history or signs of patellar instability.
The significance of lower extremity alignment
factors and pathological limits thus needs further
investigation. It is possible that the definitions used
for malalignment should be re-evaluated as the scientific support is very weak with regard to determining when alignment is normal and when there
is malalignment. Pathological limits must be clarified. Various pathological limits are stated in the
literature, indicating that if the patient exceeds various lower limb alignment measurements, this will
predispose for PFPS or indicate certain surgical
procedures. Reid[3] stated that among all alignment
measurements found in the literature, only leg length
discrepancy (not supported by Thome et al.[5]) is
249
Advancing
load
Agitation and
normal diffusion
Surface layer
low friction
Middle layer
shock absorption
Basal layer
force transfer
and absorption
Subchondral bone
Fig. 2. Three main layers of the articular surface and effects of

loading on articular cartilage permeability. An advancing load
compresses the articular cartilage and causes an expulsion of
fluid. Decreased permeability is created in the area of compression with return of normal permeability behind the advancing
load (redrawn from James,[21] with permission).
consistently found to be a significant factor in the

aetiology of PFPS.
Alignment factors are largely measured in static
positions, and not during movement. However, in
a recent kinematic CT study of the patellofemoral
joint during active flexion and extension, lateral
patellar translation and tilting was detected in 8 of
20 knees with anterior pain.[41] Using high-speed
cinematography, Dillon et al.[42] found significant
differences in gait patterns between college aged
women with symptoms of anterior knee pain compared with those without symptoms. In another study
by Powers et al.,[43] volunteers with and without
PFPS underwent gait analysis (stride characteristics
and joint motion) during level and stair walking.
Compared with the comparison group, the primary
gait compensation in the PFPS group was a reduced
walking speed, which was a function of both stride
length and cadence. It cannot be excluded that the
dynamics of the patellofemoral joint result in a
higher risk for overuse of this joint in some individuals. Any combination of malalignment and
muscle function deficit would probably increase
this risk. If this reasoning holds true, investigations
should be performed with the aim of evaluating
how much malalignment and/or muscular function
250
deficit must be present in order to increase the risk

for overuse of the patellofemoral joint during physical activity to a certain degree.
4.2 Muscular Imbalance
Muscle tightness in the quadriceps or hamstrings

has been proposed as an important factor associated with knee extensor mechanism disorders.[44]
However, measurements of the range of motion of
the hip, knee and ankle joints have not demonstrated
any significant differences between patients with
PFPS and healthy individuals.[5,23] Muscular imbalance with decreased strength because of hypotrophy or inhibition of the lower extremity muscles
has been suggested as a potential cause of
PFPS.[2,16,21,29,30,45] However, whether decreased
strength is a cause or an effect of PFPS remains
undetermined.
Decreased knee extensor strength is a common
finding in patients with PFPS,[16,23,29,30,33,45-51] and
various patterns of weaknesses have been reported.
Bennett and Stauber,[46] Werner[51] and Thome et
al.[45] found selective weakness in eccentric muscle
strength. Quadriceps electromyogram (EMG) activity can be higher and less efficient in the painful
leg compared with the non-painful leg.[52] However, Mller et al.[53] and Thome et al.[45] found
that PFPS patients had lower EMG activity than
control patients during terminal maximal knee extension in the sitting position. Selective disturbances
within the quadriceps muscle have also been suggested.[54-61] Souza and Gross,[55] studying patients
with PFPS, and Voight and Wieder,[56] studying
patients with knee extensor mechanism disorders,
suggested that an abnormal relationship between
the VMO and VL muscle activation pattern can
disturb the dynamics of the patellofemoral joint.
Many exercise treatments emphasise the importance of the VMO because of its medial pull on the
patella.[62-65] However, Cerny[54] reported that neither exercises purported to selectively activate the
VMO muscle nor patellar taping improved the
VMO : VL ratio over similar exercises. Morrish and
Woledge,[60] and Witvrouw et al.[58] reported a
reversal of the onset of VMO and VL activity in
Thome et al.
patients with patellofemoral pain, where the reflex

response time of the VL was significantly shorter
than that of the VMO. In normal individuals, significant earlier firing was obtained from the VMO
compared with the VL. In contrast, Powers et al. [59]
found no differences in the onset or cessation of
muscle activity among the vastus muscles in patients
with PFPS.
Thome et al.[45] found that the EMG activity in
the vastus medialis muscle during both concentric
and eccentric knee extension was significantly lower
in the knee angle range of 25 to 50 than the range
of 50 to 75 for the patients most and least symptomatic knee. The explanation for lower strength
and EMG activity may be that patients with PFPS
have more symptoms and pain during the last 30
of maximal sitting knee extension compared with
the 90 to 30 range.[2,3,16,21] The results from vertical jump tests reinforce the results of the knee extension torque measurements, with significant differences observed between the patients and control
individuals in a unilateral drop jump from 20cm.[45]
The unilateral drop jump, with the whole body weight
on one leg and an eccentric/concentric movement
in the knee range close to full extension, places a
very high load on the patellofemoral joint.
Some studies showed that the quadriceps EMG
activity increases in normal individuals and in patients with anterior knee pain as the knee is extended.[53,66] However, Mariani and Caruso[67] reported decreased EMG activity of the vastus medialis
muscle among 8 patients with a history of patellar
subluxation during the last 30 of dynamic knee
extension for both the affected and the non-affected side. Others have found unchanged EMG
activity, or that the EMG activity was greatest at a
90 knee angle, but with great individual variation.[19,45,68] Methods of assessment, variations in
techniques, and differences in volunteers studied
may explain these differences in results.
The significance of muscle function in a closed
vs open kinetic chain has been discussed,[15,18,69-74] but
is far from well investigated. Hungerford and
Barry[18] showed that there was a significant difference in patellofemoral joint compression forces when
loading the patellofemoral joint during standing

(closed kinetic chain) compared with sitting (open
kinetic chain). Most strength measurements of patients were made in the sitting position, and it is
uncertain how valid these measurements are for
performance in the standing position. In a study on
muscular activation in the sitting and standing positions, with great care taken in standardising the
positions, a high reproducibility at repeated tests
could be demonstrated.[75] Both the patients and
the control group produced higher isometric knee
extensor torque per knee at a 60 knee angle at
1-legged muscular activation in sitting compared
with 2-legged muscular activation in standing positions. Furthermore, there was a high correlation
between sitting and standing torque measurements.
However, no difference was found between patients
with PFPS and healthy individuals in sitting or
standing knee extensor strength measurements.[75]
Differences in activation levels can be expected
between 1- and 2-legged muscular activation as a
result of a possible central nervous system limitation to maximally activate or control all synergistic
and antagonistic muscles, as demonstrated by Secher
et al.[76] In a study of 155 male and female, untrained and trained, healthy volunteers, they showed
that the 2-legged strength was 82% of the sum of
the strength in the right and left leg. The torque
during standing position in the study by Thome et
al.[75] was 82 and 68% of the sitting torque values
for the patients and control individuals, respectively.
Closed kinetic chain exercises appear to have
gained popularity over more traditionally used open
kinetic chain exercises because many clinicians
believe that closed kinetic chain exercises are safer
and more functional.[77,78] Therefore, the importance
of using closed kinetic chain rehabilitation[79-81]
and evaluation[82,83] has been stressed. Moreover,
a recent study[84] comparing the effect of closed
versus open kinetic chain exercises on strength and
performance showed larger improvements with the
closed kinetic chain group. However, it is clear that
both closed and open kinetic chain exercises can
be useful in a PFPS training programme to minimise
the risk of excessive patellofemoral joint stress.
251
Steinkamp et al.[85] described a mathematical model

for estimating patellofemoral joint stress during
closed and open kinetic chain exercise. Patellofemoral joint stress can be minimised or increased during both types of exercise, depending on the range
of motion through which the exercise is performed.
During the closed kinetic chain exercise, patellofemoral joint stress is steadily increased as the knee
is moved from an extended position to 90 of flexion.
In contrast, during the open kinetic chain exercise,
patellofemoral joint stress is steadily increased as
the knee is moved from 90 to full extension.
In summary, based on studies available, it is
clear that further studies are necessary in order to
establish the significance of various strength deficits and muscular imbalances and clarify if a specific disturbance in muscular activation is a cause
or effect (or both) of PFPS.
4.3 Overactivity
The importance of physical activity level and

overuse has been discussed in several studies, and
it appears that the stimulus for developing and exhibiting PFPS may be related to increased physical
activity and overloading rather than malalignment
of the patellofemoral joint.[3,5,23,32,33,35] Fairbank
et al.[23] found that patients with anterior knee pain
were significantly more involved in competitive
sports than age-matched control individuals selected
from the normal population, and that pain was associated with increased physical activity. Thome
et al.[5] found that: (i) all patients reported an insidious onset of symptoms associated with temporary
overuse or a period of increased physical activity;
(ii) the patients were significantly more involved
in competitive sports than the controls. This agrees
with the findings of Fairbank et al.;[23] (iii) the patients had a significantly lower pain-free activity
level[86] than the control individuals; (iv) when
specifically asked, all patients stated that both their
maximal level of pain and their average highest
level of daily pain, as measured with a visual analogue scale, was associated with increased physical
activity; and (v) patients with a high physical activity level did not experience more pain than those
252
with a low activity level. These findings indicate

that increasing the physical activity level too drastically might result in an increased risk for developing PFPS.[5]
5. Symptoms
The most common symptoms in patients with
PFPS are pain, complaints of crepitus, giving way
and catching, occasional sensations of stiffness and
sensations of swelling.[2,5,32] Crepitus experienced
in the patellofemoral joint while flexing and extending the knee is a common symptom. However,
crepitus is not always present in patients with PFPS
and can furthermore be present without any pain or
other symptoms. Swelling is rare and, when reported, is mild and intermittent.
Symptoms of giving way can occur in patients
with PFPS with a sudden relaxation due to pain
inhibition of the quadriceps muscle during loading
of the patellofemoral joint in standing. This should
be distinguished from giving way as a result of ligamentous instability of the knee joint or meniscal
lesion during a turning movement. Giving way and
sensations of catching may be misinterpreted in determining whether intra-articular pathology is
present in the tibio-femoral joint. Fulkerson and
Hungerford[2] stated that patients with intra-articular
pathology in the tibio-femoral joint most often experience giving way while turning, and that giving
way caused by a patellofemoral problem most frequently occurs during ascending stairs or walking
down an incline.[2,5]
Catching or a locking sensation is often reported,
but is primarily transient. The sensations of catching and locking experienced by patients with PFPS
should be carefully evaluated and distinguished from
catching and locking due to intra-articular pathology.[2,3]
Unfortunately, the documentation, evaluation and
analysis of the type, duration and intensity of pain
and common clinical symptoms in different activity
situations and levels for patients with PFPS are
scarce in the literature.
Thome et al.
5.1 Pain
Pain is a common symptom in many different

musculoskeletal disorders. There are several types
of clinical manifestations of pain (such as sharp,
dull, aching, throbbing, etc.), which is why a differentiated documentation of the patients pain
symptoms can be necessary.[87] The source of
patellofemoral pain in patients with PFPS cannot
be sufficiently explained. There are no nerve endings in the articular cartilage,[88] but pain can be
elicited from the innervated subchondral bone.[2,89]
A reactive synovial change can also be a possible
source of pain but, as effusion is uncommon,[5] and
mild when present, it is less likely that the pain
arises from the synovium.[3] Fulkerson et al.[90] discussed the patellar retinacula as a potential source
of patellofemoral pain, as they found histopathological evidence of degenerative neuropathy of the
lateral retinaculum in patients with patellofemoral
retinacular tightness. Increased physical activity
could result in peripatellar soft tissue irritation and
pain may then generate from retinacular nerve endings. It is possible that malalignment factors and
overactivity may magnify this effect.[2,3,5,91]
The most common symptom of PFPS is pain
during and after physical activity, during bodyweight
loading of lower extremities in walking up/down
stairs and squatting, and in sitting with the knees
flexed.[2,3,5,21,23,30,32,92] A Visual Analogue Scale
(VAS)[47,93] has been found to be both reliable and
valid for measuring pain.[94,95] The VAS, usually
presented as a 100mm-long line with the endphrases[96] no pain and pain as bad as it could
be, correlates well with verbal scales and numerical rating scales.[97] The VAS has been found to be
more satisfactory for patient self-rating of pain intensity than 3- to 5-point verbal scales.[93,98-100]
However, Carlsson[101] questioned the basis for
these claims and found that, despite practice, patients appeared to differ considerably in their ability to use the VAS. Harms-Ringdahl et al.[102]
showed the VAS to be as reliable in assessing intensity levels of perceived pain elicited by loading
joint structures as Borgs category scale (CR-10
scale) with ratio properties for intermodal and interindividual comparisons.[103]

The VAS scores, which in principle should be
viewed as data on an ordinal scale,[93,104] can be
transformed to an interval scale by using the Rasch
analysis.[105] This allows for analysis of the hierarchical order, which is of interest in understanding
different pain-provoking situations in relation to
pain assessment according to memory, and also
gives individual measurement values with errors
for testing changes in individual patients before
and after treatment. The Rasch analysis is based on
the patients ability and on the difficulty of the item
(test situation). In a study by Thome et al.,[106] the
patients ability was replaced by the patients pain
level. The item difficulty was replaced by the value
of the pain scores on the item. The items were correspondingly positioned along a measurement line
from the most to the least pain-provoking item.
Using the VAS, Thome et al.[106] could show that
it was possible to assess pain levels in different
pain-provoking situations (items) dealing with
memories of pain, pain provoked by various tests
and pain during physical activity. The different items
were hierarchically ordered in the Rasch analysis,
illustrating the relation of the items to each other.
It was then also possible to test the significance of
changes in individual patients during treatment and
identify patients with different recovery times.
However, among activity related items, such as
descending stairs, there was a lack of items for high
level pain assessment. It was suggested that additional items should be added, such as prolonged
sitting, running on stairs, running on hilly terrain
and 1-legged jumping, to fill this gap. At the low
end of the VAS, where patients who benefit from
treatment are found, there was a similar insufficiency of low pain-provoking items that would make
the measures of low levels of pain more precise.[106]
The Rasch analysis identifies patients who report
too much or too little pain on a certain item in relation to what they report on other items. This information on the so-called misfits can be useful in
the clinic, in combination with anamnestic and clinical findings, for increasing an understanding of the
253
patients symptomatology.[106] A vertical jump test

and a dynamic strength test showed the highest frequency of misfit VAS responses. These are items
in which relatively high loads are applied to the
patellofemoral joint.
Difficulties in standardising the jump test and
varying pain expectations among patients during
the maximal dynamic knee extensor strength test
may contribute to the high frequency of responses
deviating from what was expected by the Rasch
model. Other test items, such as walking up and
down stairs, a palpation test and a compression test
appeared to be more standardised.[106] The advantages and possibilities using the Rasch analysis for
further analysing VAS scores may be of great help
for a deeper understanding of PFPS, as well as other
pain syndromes caused by various musculoskeletal
disorders.[106]
5.1.1 Strength, Pain and Inhibition
Knee extensor strength deficit is a common finding

in patients with PFPS.[16,23,29,30,33,45-51] Thome et
al.[75] showed that patients with PFPS may have a
moderate reduction of maximal motor unit activation at maximal quadriceps effort as measured during knee extension in the sitting position. Extrapolation from several submaximal levels indicated
that an additional 18% (range 0 to 58%) of knee
extensor torque could be generated. Rutherford et
al.[107] found a great variation in lack of activation
(range 5 to 95%) among 6 patients with muscle
pain of various origins. Thome et al.[75] stated that
it is likely that the estimated additional torque that
could be generated at maximal effort among the
PFPS patients is a result of reflex inhibition caused
by afferent signals from the patellofemoral joint,
as the patients also reported pain during the strength
tests. A similar use of superimposed electrical
stimulation was reported by Lindh et al.[108] in patients with chronic muscular pain (fibromyalgia).
They did not report increased pain provoked by the
maximal sitting isometric knee extensor torque
measurements, and it was therefore suggested that
the inability for maximal activation was caused by
impaired control mechanisms at a spinal or supraspinal level. Whether this explanation may be appliSports Med 1999 Oct; 28 (4)
254
cable to the PFPS patients can neither be confirmed

nor excluded, although pain inhibition is likely to
occur in PFPS patients who report increasing pain
in isometric tests.
The decreased torque and reduction in EMG activity seen in patients with PFPS, especially during
eccentric knee extension, may imply quadriceps inhibition selective to heavy patellofemoral loading
such as eccentric knee extension and vertical jump
on one leg.[45,46,51] These effects seem to appear
specifically at knee angle ranges close to full extension and in the vastus medialis muscle.[45,53,55,109]
Inhibition and ability to develop torque in different
situations should be taken into account when developing treatment programmes for patients with
PFPS. Further studies should be performed to analyse the presence and impact of reflex inhibition.
5.1.2 Personality and Pain
With chronic pain as a dominant factor in PFPS,

greater attention has been focused on the relationship between personality and pain. Carlsson et al.[110]
discussed pain behaviour in patients with long term
PFPS and stated that chronic pain most often has a
multifactorial origin, and that the significance of
the psychosocial, social and biological factors may
vary. By observing the patients facial expressions,
posture, verbal expressions and pain reactions on
different provocation tests, information can be attained regarding pain behaviour. Certain pain
behaviours may be more likely to recur or persist
because of their effects, while others may occur
less frequently or less intensely because reinforcing events no longer occur. Improvement in the
pain experience may follow an improvement in
functional abilities and activities.[110-113] Carlsson
et al.[110] found only a few significant differences
between knee patients and control individuals using several methods assessing anxiety, depression,
helplessness, aggression, hostility, passive attitudes
and alexithymic characteristics.
If the patient behaves as though he or she experiences significant pain and there is an absence of
adequate physical findings that might account for
this pain, it is a frustrating situation for both the
clinician and the patient. The pain behaviour of the
Thome et al.
patient is sometimes presumed to stem from some

kind of personality, emotional or motivational difficulty. When that assumption is made, the clinician often thinks of the patients pain as not real,
or as exaggerated or malingered. The implication
is that the patient is not really suffering.[111,114]
This latter feeling is often made apparent to many
patients with PFPS, not only by clinicians but also
by parents, peers, teachers, etc.[5] The prevalence
of any personality, emotional or motivational problems among patients with PFPS is not well documented.
6. Treatment
Basic knowledge is lacking and no strong scientific evidence has been presented in the literature on
the nature and aetiology of PFPS. This could explain
why there are so many treatment protocols described
in the literature.[15,62,70,71,109,115-125] However, Arroll
et al.[124] found only 5 randomised controlled trials
in their extensive review on non-operative therapy
for PFPS, and concluded that there is little evidence
on which to base therapy. The number of patients
experiencing PFPS are numerous and decisions
still have to be made daily, throughout the world,
on how a treatment programme should be set up for
these patients. We suggest a comprehensive approach
that can account for the complexity that PFPS presents us with.
Shelton and Thigpen[121] argued for avoiding a
cookbook approach and advocated a biomechanical approach. Progression should be achieved without increasing symptoms. Key factors in a training
programme are: strength, flexibility, proprioception, endurance, functional training and a gradual
progression of the exercise load.[62,70,121,122,109]
Another important factor is compliance, stressed
by Yates and Grana,[126] who found at 15-month follow-up in 64 patients that 42 were non-compliant,
17 partially compliant and 5 compliant with the
prescribed exercise programme. Surgical treatment
is rarely indicated,[71,109,127-129] and the most frequently recommended treatment for PFPS is an exercise programme.[15,70,71,109,121] The natural
course of 48 patients with PFPS given information
and an isometric training programme, when followed up after a mean period of 11 years, was
found to be excellent or good in 85%.[34] This
agrees with the findings of other studies.[129,130]
However, the effects of an exercise programme for
PFPS are not well documented. Various results (50
to 100% success rate) are reported, as well as variability among studies in the diagnoses, physical activity level, gender and age of the patients.
The following studies, all with limited scientific
evidence, present a spectra of various treatment approaches. Kannus and Niittymki,[33] ONeill et
al.,[131] and Werner and Eriksson[122] studied male
and female patients with PFPS and reported good
results from an exercise programme, while others[11,46,70,132] studied patients with anterior knee
pain with different possible underlying diagnoses.[3]
The earliest study in the literature, by DeHaven et
al.,[11] presented a prospective analysis of 100 athletes with the clinical diagnosis of chondromalacia
patellae. Eighty-nine percent of the athletes were
able to return to athletics after a treatment programme
consisting of: (i) symptomatic control; (ii) a progressive resistance programme of isometric quadriceps and isotonic hamstrings exercises; (iii) a graduated running programme; and (iv) a maintenance
programme.
Hrding[24] treated 34 students between 8 and
19 years of age with isometric training for those
with moderate complaints and a soft brace for those
with more serious complaints. After 4 months, 50%
of the students were symptom free. In a study by
Bennett and Stauber,[46] all 41 patients recovered
their eccentric strength in 4 weeks using eccentric
isokinetic exercises. After a 12-week treatment programme for patients with chondromalacia patellae,
McMullen et al.[132] could not find any difference
between an isometric and an isokinetic exercise
programme. Both programmes demonstrated significant functional improvements over a control
group receiving no treatment. ONeill et al.[131] found
that 80% of patients with PFPS were improved at
a follow-up 12 to 16 months after an isometric
strengthening programme that included stretching
exercises. Doucette and Goble[70] had an 84% suc Adis International Limited. All rights reserved.
255
cess rate of pain-free patients after 8 weeks of an

individualised, comprehensive, 5-stage physical
therapy programme including stretching, and isometric and dynamic strengthening exercises in both
open and closed chains.
Werner and Eriksson[122] found a significant
improvement in patients with PFPS in maximal concentric and eccentric knee extensor torque after 8
weeks of isokinetic training. The measurements and
training were performed in the sitting (open kinetic
chain) position. Kannus and Niittymki[33] showed
complete recovery in 70% of patients with PFPS,
with a reduction of physical activity level by the
elimination of all symptom-producing activities,
enforcement of a quadriceps strengthening programme and the use of nonsteroidal anti-inflammatory medication. Stiene et al.[133] compared closed
kinetic chain and isokinetic joint isolation exercise
(open kinetic chain) in patients with patellofemoral dysfunction. They found that both groups had
significant improvement in an isokinetic knee extension test, but only the closed kinetic chain group
showed significant improvement in closed kinetic
chain testing and perceived functional status.
Thome[109] presented a successful comprehensive treatment approach for PFPS. The approach is
based on standardised information, a pain monitoring
system and an exercise programme with a progression plan allowing for the individually and specifically designed treatment approach advocated in
recent studies.[3,15,70,71,121,134-136] A significant reduction in pain and improvements in strength and
physical activity level were seen after 12 weeks of
treatment. Furthermore, all 40 patients had significantly less pain, as analysed with the Rasch analysis, at the 12-month follow-up compared with before
treatment. At the 12-month follow-up, 90% of the
patients were engaged in competitive or recreational
sports without pain and 39 patients, 2 of whom had
undergone surgery (lateral retinacular release), rated
their knee function as excellent or good. Reasons
for improvement may be an effect of time, the
standardised information, the pain monitoring system, the gradually progressive training programme
and the adjusted physical activity level. The study
256
lacked a proper control group receiving no treatment, which limits the possibilities for evaluating
the effects of treatment. However, the patients
were retrospectively their own controls, having an
average of 8 months of rest without relief of symptoms. Thus, time is not likely to be a major cause
of the improvement.
It is likely that the standardised information results in a better understanding of PFPS and that the
information given may have contributed to an altered physical activity pattern. The patients were
allowed to continue, using the pain monitoring system, with adjusted physical activity during treatment. This resulted, for example, in an avoidance
or reduction of temporary heavy loading of the
patellofemoral joint.
In the study by Thome,[109] no significant differences in physical activity levels, pain and muscle
function were found between the 2 training groups.
Thus, the treatment effects do not seem to be sensitive to a particular choice of exercise in the training
programme. A reduction in pain that lasted through
and for 1 to several hours after the training programme was reported by most patients after a 10 to
15 minutes of training. Thus, the author speculated
that the exercises used may have modified the inflow of afferent signals with reduced reflex inhibition and possible effects on the endorphin system.
Better muscle activation, with increased motor unit
recruitment as well as a more normal activation of
the vastus medialis muscle, may thus be achieved.
The training programme used by Thome[109]
might also result in an increased diffusion of nutrients to the cartilage caused by loading and unloading the patellofemoral joint,[21,135] and improved
nutrition to surrounding joint structures and muscles owing to increased blood circulation. Thus, it
may be anticipated that the training programme
yielded positive effects on the patellofemoral joint
structures, as adaptive changes can be seen in muscles, tendons, ligaments and the cartilage after regularly repeated, slowly progressing, non-strenuous
physical training.[124,137-140] However, this reasoning
is only speculative, with limited scientific support.
Exercises that are too strenuous or biomechanic Adis International Limited. All rights reserved.
Thome et al.
ally unfavourable may cause a gradual breakdown

of the musculoskeletal tissue, articular cartilage being the most sensitive of these,[138] which emphasises the need for a carefully controlled training
programme. The increased physical activity after
treatment may contribute to the further improvements in symptoms and muscle function seen at the
12-month follow-up.[109]
In this study, a pain monitoring system was used
allowing for pain evaluation and monitoring in
which pain during and after exercise or physical
activity was permitted. This is in contrast to recent
review articles on the treatment of patellofemoral
pain, which advocate that all training should be
done pain free.[3,121,134-136] Thome[109] argued that
it is likely that maintaining a level of no pain during
or after physical activity for patients with PFPS
requires such a decrease in physical activity and
loads during treatment that improvements may fail
to appear. However, the acceptance of a level of
pain that is too high can result in immediate and
frustrating setbacks. The pain monitoring system
used by Thome[109] allowed for gradual exercise
progress with minimal risks for overloading and
overuse of the patellofemoral joint. As patient
compliance was very high and there were no dropouts, use of the pain monitoring system is advocated in the treatment of patients with PFPS.[109]
6.1 Patellar Taping
The recommended approach to taping for patellar

malalignment cited in many recent articles[62] was
not considered in the study by Thome,[109] as the
patients in that study had no signs of patellar malalignment. A recent study[141] reported poor to fair
reliability among 12 physical therapists, comparing
a series of patellofemoral alignment tests to determine when and how patellofemoral taping techniques should be used. This was not surprising, as
patellar malalignment is a questionable characteristic
of PFPS.[3,5,23,32,33] Werner et al.[142] found that patients with patellar hypermobility increased their
knee extensor torque with taping. However, Cerny[54]
could not improve the EMG activity ratio between
the VMO and the VL muscles using patellar taping.
Positive effects of the McConnell[62] approach,

including taping and a functional lower extremity
exercise programme, might be found in factors discussed above and not necessarily be the result of
the specific taping techniques used. Kowall et
al.[143] evaluated the results of a physical therapy
programme that used patellar taping in a group of
patients with PFPS. These results were compared
with results from a similar group of patients who
underwent a physical therapy programme without
patellar taping, and suggested no beneficial effect
of adding a patellar taping programme to a standard physical therapy programme in the treatment
of patellofemoral pain. Using the McConnell[62]
medial glide patellar taping technique, Larsen et
al.[144] showed that taping was effective in significantly moving the patella medially, but that the tape
was ineffective in maintaining this significance
after exercise.
Gilleard et al.[61] investigated the effect of patellar taping on the onset of activity of VMO and
VL. Fourteen female patients with patellar pain
walked up and down stairs in 2 conditions: (i) with
the patellofemoral joint of the painful lower extremity taped so that the pain was reduced by at
least 50% on a pain provocation test; and (ii) without patellar taping. When the patellofemoral joint
was not taped, there was no difference in the onset
of activity between the VMO and VL during the
step-up and step-down tasks. In contrast, when the
patellofemoral joint was taped, the VMO was activated earlier than the VL during the step-up and
step-down tasks. The authors concluded that the
earlier activation of the VMO may alter the movement of the patella, and that further research is
needed to determine whether this occurs and
whether it is beneficial.
6.2 Surgical Treatment
Although non-operative treatment is always

preferable for PFPS as the primary treatment, more
than 100 surgical procedures have been described
for the treatment of patellofemoral disorders. Most
of these operations, rarely evaluated with randomised
controlled studies, are directed at treating malalign Adis International Limited. All rights reserved.
257
ment (often called realignment procedures) or other

abnormalities of the extensor mechanism, or aimed
at treating injured cartilage.
Lateral retinacular release. This procedure can
be performed alone or in combination with other
realignment procedures. The main surgical indications are: (i) excessive lateral compression syndrome
with tenderness and tightness of the lateral retinaculum, combined with lateral patellar tilt; (ii) patellofemoral osteoarthrosis with lateral patellar tilt; and
(iii) persistent patellofemoral pain combined with
a lateral traction osteophyte at the insertion of the
lateral retinaculum into the patella.[145] This procedure is not recommended for very young patients,
or for patients with advanced patellofemoral osteoarthrosis and normal patellar tracking. The results
after this procedure have been unpredictable, with
a reported rate of satisfactory results between 20
and 92% of patients.[146] Furthermore, biomechanical studies have not shown any effect of this
procedure on the patellofemoral contact area or the
muscular forces around the knee.[147]
Proximal realignment procedures. Several different techniques for proximal, soft tissue realignment have been described. The most common is a
modification of the technique described by Insall
et al.[148] These procedures are mainly indicated in
patients who: (i) are skeletally immature and have
a history of recurrent dislocations; (ii) are skeletally mature or immature and have an increased
congruence angle combined with patellofemoral
pain; and (iii) have dysplastic femoral trochlea and
poor medial patellar support of the VMO muscle,
causing recurrent patellar subluxations or dislocations. Even though satisfactory results have been
reported in 79 to 91% of patients, these procedures
are now rarely used.[149]
Distal realignment procedures. These procedures
are most commonly used for recurrent patellar subluxation or dislocation and less for patellofemoral
pain. Several modifications of tibial tubercle transfer have been described. The indications for these
procedures are; (i) persistent patellofemoral pain
combined with excessive patellar tilt or subluxation or increased congruence angle; (ii) lateral
258
facet osteoarthrosis combined with a high Q angle;

and (iii) failed lateral release procedure, especially
in patients with significant lateral tilt or subluxation. This procedure should never be performed in
skeletally immature patients, because of a risk of
development of genu recurvatum.[150] Satisfactory
results have been reported in 80 to 96% of patients
after different distal realignment procedures.[151]
However, concerns have been raised about the long
term results.
Elevation of the tibial tubercle. Biomechanical
studies have shown a 50 to 83% decrease of patellofemoral compression force after elevation of the
tibial tubercle of 1.2 to 2.5cm.[152,153] The main indication for this procedure is moderate chondromalacia patellae (degeneration of the cartilage) or
osteoarthrosis that does not respond to non-surgical
treatment. Satisfactory clinical results have been
reported in 30 to 95% of patients treated with this
procedure,[154] and complications in 18 to 40%. As
the results have been very unpredictable and the
long term results unsatisfactory, this procedure is
now rarely used for patellofemoral pain.[155]
Anteromedial tibial tubercle transfer and elevation. This procedure has been advocated by Fulkerson[156] for patients with malalignment, an increased
Q angle, and mild-to-moderate osteoarthrosis. The
results have been reported as satisfactory in 75%
of patients after 5 years.[156]
Articular cartilage procedures. These procedures
include open or arthroscopic patellar shaving, local
excision of defects with drilling of the subchondral
bone, facetectomy and transplantation of autologous
chondrocytes. The major benefit of arthroscopic
interventions might be the lavage with removal of
debris from the knee joint. Local excision of diseased cartilage and subchondral drilling has been
used very commonly, even in patients with severe
chondromalacia of the patella. Satisfactory results
are achieved in several patients, especially below
the age of 25 years.[157] No comparative studies on
these procedures are available and the results are
often considered to be satisfactory in the short term,
but less is known about the long term outcomes.
Thome et al.
Patellectomy. This should be considered as the

last resort for treating patellofemoral diseases as it
often results in a considerable decrease in functional ability. The main indication for patellectomy
is severe patellofemoral pain after failed realignment procedure in a patient younger than 40 years.
Contraindications are tibial-femoral disorders and
patellofemoral pain of unknown cause.[158]
7. Conclusion
When individuals remain disabled for long periods despite a variety of treatments, and when the
disability diminishes when a new method is tried,
the inference can be drawn that the new treatment
is more effective. However, it may be difficult to
determine what the active ingredients are in a
complex treatment programme. Thome[109] argued
that the reasons for improvement with the comprehensive treatment approach used may be found in
the standardised information given, the pain monitoring system, the specified gradually progressing
training programme and adjusted physical activity.
PFPS is multifactorial, and thus it is likely that all
of the abovementioned reasons are active ingredients.
It seems most likely that standardised information and adjusted physical activity will be sufficient
for many PFPS patients having mild symptoms.
Avoiding abuse of the knee, avoiding pain-causing
activities such as heavy loading of the patellofemoral
joint, i.e. excessive stair walking or squatting, and
avoiding prolonged sitting with knees flexed could
be recommended. However, there is no reason why
patients with PFPS should give up their physical
activity. On the contrary, adjusted physical activity
seems important. For patients who have had PFPS
for more than 6 months, a detailed, specified training programme using a pain monitoring system
could be recommended.[109]
Another key word in the treatment of patients
with PFPS is patience. Improvements come slowly,
especially at the beginning of the treatment period,
and the positive effects of training on musculoskeletal tissue take time. It seems important that the
training programme gradually progresses in load
and the exercises used. The success of the treatment can also depend on the therapists ability to
adjust the various exercises of the training programme in relation to the patients specific symptoms and needs.
It is strongly suggested that, when presenting
reports on PFPS, a detailed description should be
provided of the diagnosis, individuals studied (inclusion and exclusion criteria), and methods in order to understand the conclusions drawn and be
able to compare results with other studies. As this
is not the case in most studies on PFPS found in
the literature, it is only possible to make general
comparisons. In order to further develop treatment
models for PFPS we advocate prospective, randomised, controlled, long term studies using validated
outcome measures. However, there is a strong need
for basic research on the nature and aetiology of
PFPS in order to better understand this interesting
syndrome.
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Correspondence and reprints: Dr Roland Thome, Muscle Laboratory, Department of Rehabilitation Medicine, Sahlgrenska
University Hospital, Sahlgrenska, Guldhedsgatan 19, 41345
Gteborg, Sweden.
E-mail: roland.thomee@telia.com

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REVIEW ARTICLE

Sports Med 1999 Oct; 28 (4): 245-262

Patellofemoral Pain Syndrome

decreased strength due to hypotrophy or inhibition have been suggested, but

1. Definition of Patellofemoral Pain

The term anterior knee pain is suggested to

Patellofemoral Pain Syndrome

Table I. Pathologies that can generate anterior knee pain

Peripatellar tendinitis or bursitis

Menisci, ligament and capsular damage

Sequelae after patellar fracture, dislocation or subluxation

Iliotibial band friction syndrome

Sequelae after knee surgery

Pre- and infrapatellar bursitis

toms as well, and thus it is appropriate to use the

The patellofemoral joint consists of the patella,

The cartilage has viscous and elastic properties,

Among 15 year olds, the incidence was 10%. The

of the cartilage, and synovial fluid diffuses into the

Malalignment of the lower extremity has been

Patellofemoral Pain Syndrome

once it has been acquired, but this is not very well

The shape of the patellar and femoral surfaces,

Fig. 2. Three main layers of the articular surface and effects of

consistently found to be a significant factor in the

deficit must be present in order to increase the risk

Muscle tightness in the quadriceps or hamstrings

patients with patellofemoral pain, where the reflex

Patellofemoral Pain Syndrome

loading the patellofemoral joint during standing

Steinkamp et al.[85] described a mathematical model

The importance of physical activity level and

with a low activity level. These findings indicate

Pain is a common symptom in many different

Patellofemoral Pain Syndrome

scale) with ratio properties for intermodal and interindividual comparisons.[103]

patients symptomatology.[106] A vertical jump test

Knee extensor strength deficit is a common finding

cable to the PFPS patients can neither be confirmed

With chronic pain as a dominant factor in PFPS,

patient is sometimes presumed to stem from some

Patellofemoral Pain Syndrome

cess rate of pain-free patients after 8 weeks of an

ally unfavourable may cause a gradual breakdown

The recommended approach to taping for patellar

Patellofemoral Pain Syndrome

Positive effects of the McConnell[62] approach,

Although non-operative treatment is always

ment (often called realignment procedures) or other

facet osteoarthrosis combined with a high Q angle;

Patellectomy. This should be considered as the

Patellofemoral Pain Syndrome

Adis International Limited. All rights reserved.

16. Ficat R, Hungerford D. Disorders of the patello-femoral joint.

Sports Med 1999 Oct; 28 (4)

39. Stanford W, Phelan J, Kathol MH, et al. Patello-femoral joint

Adis International Limited. All rights reserved.

59. Powers CM, Landel R, Perry J. Timing and intensity of vastus

Sports Med 1999 Oct; 28 (4)

Patellofemoral Pain Syndrome

81. Callaghan MJ, Oldham JA. The role of quadriceps exercise in

Adis International Limited. All rights reserved.

Sports Med 1999 Oct; 28 (4)

127. Evans TK, Paulos LE. Complications of patello-femoral surgery.