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European Federation of National Associations of

Orthopaedic Sports Traumatology

E-Newsletter | Volume # 6 | October 01, 2010 (Supplement)

1992
Official address: Rue Froissart 38, 1040 BRUSSELS, BELGIUM
info@efost.org, www.efost.org
account nr 001-5296161-37, IBAN BE 35 001529616137, BIC GEBABEBB, bank FORTIS

EDITOR
M. N. DORAL MD, TURKEY

CO-EDITOR
G. MANN MD, ISRAEL

BOARD of EFOST
PRESIDENT J. F. HUYLEBROEK MD, BELGIUM
GENERAL MANAGER H. DE BOCK, BELGIUM
VICE PRESIDENT F. KELBERINE MD, FRANCE
TREASURER M. N. DORAL MD, TURKEY
PAST PRESIDENT F. BENAZZO MD, ITALY

MEMBERS
F. ALMQVIST MD, PhD, BELGIUM
GL. CANATA MD, ITALY
C. ESTEVE DE MIGUEL MD, SPAIN
R. HACKNEY MD, ENGLAND
B. KLOS MD, THE NETHERLANDS
N. MAFFULLI MD, ENGLAND
G. MANN MD, ISRAEL
P. PAPADOPOULOS MD, GREECE

EASTERN-EUROPE REPRESENTATIVE: A. GLUSHENKO MD, UKRAINE


SCIENTIFIC SECRETARY S. KARAOGLU MD, & R. TANDOGAN MD, TURKEY

ADVISORY COMMITTEE
M. CARMONT MD, UK - G. DONMEZ MD, TURKEY
M. RAUH MD, USA - B. WIND MD, USA
EDITORIAL

Dear Colleagues,

Here we are again with the October Vol 6 Supplement Newsletter after three
months. First of all, on behalf of EFOST Board I wish to thank Dr. G Mann for his
great effort to get complimentary permission from American Academy of Pediatrics
for their great paper “Anterior Knee Pain Syndrome” was published in Adolescent
Medicine to add new issue of Newsletter. And also special thanks to Dr. R. Debi for
the abstract summary that he prepared for us. Enjoy them...

As you will see at the following pages of Newsletter, 6th EFOST Meeting is getting
closer. The 4th one was in Pavia and the 5th in Antalya in November 2008. I know,
my friend Mr. President Dr. José Huylebroek, Organising and Program Committee
are still working all day and night. Then I would like to give my respects to Dr.
William G. Clancy and Dr. Rene Verdonk as “Honorary Presidents”. Also my old
friends Dr. John Bergfeld, Dr. Mitsuo Ochi and Dr. Savio Woo will honour all of us
with their kind contribution and high-level scientific lectures. As President says
EFOST 2010 promises to be the year’s leading meeting on sports traumatology.
Comprehensive Congress Program including 25 lectures, 18 special and mini-
symposiums, 5 video sessions, 3 debates and free papers also seems so exciting
and promising for the best EFOST Meeting ever. Although EFOST 2010 will specially
focus on osteoarthritis in the young patient and first time shoulder dislocation, a
large spectrum program on sports injuries accompanied with radiological
symposiums and physiotherapy sessions, improve the expectations.

Please do not forget to submit your abstracts until middle of October and visit
congress website www.efost2010.com for detailed information. We are all looking
forward to welcoming you to EFOST 2010 and to the “Capital of Europe”, Brussels.

Dear President Dr. Huylebroek, I believe that the Congress of “Brusells EFOST
2010” will be the best of the year on sports traumatology. Congratulations in
advance.

Mahmut Nedim DORAL, M.D.


Editor
PRESIDENT REFLECTIONS

September 2010

This is my last contribution to the EFOST newsletter as the President of EFOST.

So I thought I would give you my impression on the past 3 years. The most
striking fact for me is that these 3 years of Presidency (You might remember that
Prof Benazzo had to leave the post of President rather early, due to his
overwhelming work in his new job as responsible chief of Orthopaedics at the
University of Pavia) passed by so quickly! That means that the years of Presidency
were exciting, very well filled in and full of challenges.

Let’s make a quick journey of the different items I wanted to achieve and of what
the final review could be of my presidency.

A lot of societies, enterprises or associations couple their success with their


financial status. Today, with our treasurer Prof MN Doral, and our General Manager
Mr H De Bock, I can say that the financial situation of EFOST is stable, sound and
well structured. Of course, and that was one of my statements at the beginning of
my legislature, the relationship with the Medical Industry has reached its maturity:
today we have good support from the major Orthopaedic companies, either as a
privileged partner or as a dedicated sponsor for our educational activities.

Of course we cannot accept to stay on the same spot: stagnation means decline. A
lot of work still needs to be done in this field, particularly all over Europe. Probably
one of the nicest jobs as Your President, has been the representation of this Sports
medicine group at different occasions, on many meetings.

Not only the full recognition of our association by f.i. AAOS, ISAKOS, ESSKA etc.
was worth the immense work of preparation speeches and talks, but also the
invitations by small private meetings, national or regional societies all over the
globe brought us to places we would never have been without that sort of
meetings.

Maybe the most wonderful experience for me, was the warm hospitality of so many
different groups of professionals and individuals: if it was the CEO of a big
pharmaceutical company, the governor of Health of a small country in Africa or a
group of enthusiastic physiotherapists in Turkey, the constant determinant was the
feeling that EFOST means something for so many people.

I must thank you all that you have given me the opportunity to go through this
type of experiences.

One of the major achievements I would like to mention, is the “ mise au point” of
the EFOST-DJO travelling fellowship. Recognizing the immense work of Dr F
Kelberine, today we can say that the fellowship is well organised, very popular for
young surgeons and the reports post-fellowship prove the unique once-in-a –life-
experience for the elected fellows.

The hands of Dr G Mann and Prof MN Doral are very well visible when you look at
www.efost.org and particularly when you read the more and more regular E-
newsletter, our preferred way of communication with the members on the field.

Prof F Almqvist and Dr Ph Landreau, the two program chairmen of the upcoming
6th European congress of EFOST in Brussels, have prepared an outstanding
program for the meeting at the end of November 2010: have a look at
www.efost2010.com and you are immediately convinced about the amount of new
stuff we will have to assimilate later on this year. EFOST, together with the GCO
company, the organisers of the meeting, are waiting for your registration.

For the first time in an EFOST meeting, we have included a few EAST MEETS
WEST” meetings: experts from Eastern Europe will discuss and debate with
speakers from Western Europe about common topics: our Eastern European
colleagues, who register at a reduced fee, can ask questions in their own language.
Bringing Eastern Europe again closer to Efost was one of my great wishes since the
beginning of my Presidency: our good contacts today, not only with Poland, but
also with Ukraine, Russia, Slovenia, Lithonia, etc have proven our successful
promotional work in these countries. With the help of the Pharmaceutical Industry,
we hope to start next year, regional instructional courses.

London is the place to be in 2012: the Olympic games and the World congress on
Sports trauma, co-organised with EFOST: we wish the English organisers and good
friends, Prof N Maffulli, Mr R Hackney and Mr M Carmont great success and a
fantastic meeting in London, at the end of 2012.

At the General Assembly, to be hold during the upcoming congress in Brussels,


some changes in the bylaws, particularly about the Executive Board and the Board
At Large, will be voted. Please join us for that meeting. But a lot of work still has to
be done: I am a bit disappointed not to have been able to reorganise the
Delegates’ group: we still have to work on “ duties and rights” of the national
representatives. A closer contact with quite a few national societies is another
critical item for the future. And still, although all of the Board members have been
travelling extensively, in some European countries, even some of the larger ones,
Efost has not yet a full representation in the Sports medicine world of that area.

I would say, some interesting challenges for your next president, Dr F Kelberine: I
wish him every success. I am sure that EFOST will go from strength to strength
under his leadership.

Finally, I would like to thank the wonderful group of friends, the Board At Large,
who supported and helped me a lot during the last years: it has been a pleasure
working together with such a group of International experts: they really became
very good friends. It would have been an impossible job without their support and
wise council.

I must thank my wife Martine and my four children, Barbara, Karolien, Charlotte
and Sam, as it has been a difficult period for us, as many of you may be aware.
Without their love and support I may have had big trouble to continue.

But, to end with the wise words of Mike Bells, the former BOA president,

“Happily, I survive to fight another day…”

It has been a privilege and a pleasure to have served as your president!

J. Huylebroek M.D.

EFOST President (2007-2010)


ANTERIOR KNEE PAIN SYNDROME

Gideon Mann, MD1,3, Naama Constantini2, Iftach Hetsroni, MD3,


Omer Mei-Dan, MD3, Eran Dolev, MD3, David Morgenstern, MD3,
Ayala Mann, MSc, Meir Nyska, MD3

1
The Ribstein Center for Research and Sports Medicine, Wingate Institute,
Netanya, Israel.
2
The Department of Orthopaedic Surgery, Hadassah University Hospital,
Jerusalem, Israel.
3
The Meir Medical Center, Kfar Saba, Israel.

Correspondence: Gideon Mann, M.D.


e-mail: drmann@regin-med.co.il
Tel: 972-2-6511220, 972-52-251-4608

*** Printed with permission from the American Academy of Pediatrics:


Adolescent Medicine: State of the Art Reviews

"Anterior Knee Pain Syndrome" (AKPS) would best be defined as a painful condition
arising in or around the patello-femoral joint, insidious in onset, bilateral, with no
macroscopic gross pathology. Anterior Knee Pain as a descriptive term would
define the need to search further for a specific cause of pain (229,230), as neither
patellar cartilage damage (231) nor Malalignment (19,86,109,116, 230), would
necessarily be correlated to pain.

The examining physician should be aware that specifically in adolescents the higher
chance would be that eventually no clear-cut pathology would be found and thus,
great caution should be taken before diagnosing AKPS as existing unilaterally. It
could be claimed, following the above, that as apposed to the term "Anterior Knee
Pain", the term "Anterior Knee Pain Syndrome (AKPS)" is an exclusion diagnosis,
applied after Macroscopic pathology has been ruled out (298).
Introduction:

Anterior knee pain is the most frequent occurring disease of the knee. 17% of a
patient population visiting a hand injury clinic declared of suffering from anterior
knee pain (115). The condition is frequently observed in children and in
adolescents (240). 30% of school children in one school year have been reported
as suffering from anterior knee pain (116). In the military, anterior knee pain
syndrome occurs in 15-30% of recruits (41,86,117,219,272) rising to 50% in
specific high demand units (118) or 60% in exceptionally physically demanding
military courses (111,119).

The term AKPS may be misleading as the pain is often neither constant, nor well
localized (232). The onset of pain could be gradual or follow a physical stressful
event (232), and its location though most often pre-patellar, may be para-patellar,
posterior, or located on the Medial Joint line in up to 30% of cases (232,273).
Thus, AKPS could imitate other internal knee derangements, especially as other
"classic" symptoms as Crepitos, Giving-Way, Locking and Swelling are not unusual
(230). In the AKP patient, though, these symptoms should be interpreted with
caution (230).

Anatomy:

On flexion the patella comes in contact with the femur from below upward until at
135° flexion only the lateral and medial aspects of the patella will contact the
femur (53,84). At 90° flexion the quadriceps tendon will contact the femur and
thus take its role in reducing patella-femoral joint pressure (53,84). The normal Q
angle (Quadriceps Angle) reaches 10° in men and 15° in women (19,120) and may
differ according to the foot position (67). When measured in flexion the QA is
normally 0° and abnormal when over 10° (121). Others described a Q angle of
approximately 13° for men and 16° for women, which increases by about 1° in the
standing position (220). The lateral force imposed on the patella by the QA is
balanced by the medial pull or the oblique part of the vastus medialis muscle (66).
Diagnosis and Differential Diagnosis:

Anterior Knee Pain Syndrome patients most commonly, complain of vague,


bilateral pain, insidious in onset and aggravated by stair climbing, descending or
prolonged sitting (99,122,230,232). Unilateral complaints must always raise the
suspicion of a diagnosis other than Anterior Knee Pain Syndrome (298) such as
patellar instability, Osgood Schlatter, peripatellar syndrome or direct trauma all
which should be seeked by history and physical examination (122). Anterior knee
pain syndrome carries a wide differential diagnosis (123,232,230). This would
include almost any knee disease causing knee pain which should be probably
excluded before the final diagnosis of AKPS is applied.

Etiology:

A good correlation has been shown between the physical finding and the patients
complaints (123). A wide variety of causes are mentioned in the literature as
possible causes of anterior knee pain. The most often mentioned is over use with
no definite observed anomaly (116,124,240).

Biedert et al in 1992 (234) demonstrated nerve endings in the Patellar Tendon, the
Retinaculum, the Pes Ancerinus Tendons, the Synovium and the Fat Pad. Similar
findings were demonstrated by Witonski & Wagrowska-Danielewicz in 1999 (239).
Dye in 1998 (193,235) showed by arthroscopy of his own knee the major pain
sensitive structures to be the Fat Pad and the Synovium, with much less pain
sensation located to the Articular Surfaces, the Menisci and the Ligaments.

Various sources have been claimed to cause Anterior Knee Pain. These would
include cartilage degeneration or osteoarthritis (125,126,127,128,129,130,131,
132,133,134,147,149,233), nerve tissue or Neuromata in the lateral retinaculum
(48,135,226,233,236,237,236,238), excessive lateral pressure or hypertrophic,
tight and painful lateral retinaculum (43,44,45,46,47,122,136,137,148,174,175,
221,233,237,238) (Fig 1). Accordingly a surgical procedure has been suggested by
Kasim & Fulkerson in 2000 (241) in which painful sections of the retinaculum were
resected with satisfactory results.

Sympathetic dystrophy of the patello-femoral joint (RSD) which would be disclosed


by a positive bone scan (138,139,140,141,142,143,222,223,224,225,233) (Fig 2),
has been repeatedly mentioned as a cause of AKPS, and is further discussed below.
Uncoordinated reaction of the muscles with the vastus lateralis firing before the
vastus medialis while the vastus medialis is normally the first to fire was originally
described by Voight and Wieder in 1991 (144), further developed by Cesarelli in
1999 (244), by Witvrouw in 2000 (245), by Cowan in 2001 (242), and by Owings
in 2002 (243).

Low flexibility of the Quadriceps, Gastrochemius and Hamstring muscles (145,


226,245), and low force and low electric activity of the Quadriceps especially on
blasting force (150,245,246) have been seriously considered as major contributing
factors. Other causes that should be kept in mind concern various other internal
knee derangements as an intermeniscal fibrous band (151), a ganglion cyst in the
ACL (152,153), a supra-patellar membrane (51,52), pinching of the synovium
under the patella (49,50) [though, synovium in the patello-femoral space has
been shown as a normal occurrence (69)], patellar or quadriceps tendinitis (70,75,
247), Hoffa's disease representing injury and fibrosis of the fat pad (71,163,164,
165), stress fractures (76) or bipartite patella (166,167,179) (Fig 3). Unusual
causes described are retro-patellar calcification (248), Quadriceps Tendon Cyst
(249), softening of the Synovial bed in the proximal groove (250), Safenous Nerve
Entrapment (146), the Sindig-Larsen-Johansen Syndrome or proximal patellar pole
Apophysitis in children or adolescents (251) or Dorsal Defect of the adolescent
patella (251).

We should elaborate slightly on some of the more controversial etiologies:


The Plica Syndrome:
The Plica Syndrome which is the occurrence of an abnormally thick or fenestrated
(hollowed) synovial fold warrants specific mentioning as the fold often occurs in the
normal knee. When other pathology has been excluded it would be justified to
remove the plica, a procedure which occasionally gives good results (130,198,199,
200).
Fig 1: Lateral tilt in a normal and subluxing patella as seen on a skyline view:
A: Normal positioned patella

B: Lateral tilting patella

The tilt is caused by a tight lateral retinaculum

Proprioception:
The relation of Proprioception to AKPS is little discussed and ill defined. Baker et al
in 2002 disclosed Proprioception to be defective in AKPS (279) though it remains
unclear whether this is a cause or a result. The possible relation of his finding to
core stability as discussed below should also be kept in mind.
Fig 2: Sympathetic Dystrophy of the right patella: Intense uptake on the bone scan
A. Anterior-Posterior view

B. Lateral view
Fig 2: Sympathetic Dystrophy of the right patella: Osteoporosis on the x-ray
C. Both Knees - only left affected

D. Left Knee

Anterior Knee Pain after ACL Reconstruction:


After ACL reconstruction, various reasons could cause anterior knee pain syndrome
as roof impingement of the reconstructed ligament (154) or damage to the
extensor mechanism when using the patellar tendon as a graft (92,155,156,157,
158) though it should be mentioned that macroscopic damage to the patella was
found by Tria in 24% (155) and by Krahl in 33% (91) of patients already at the
time of operation for ACL reconstruction. Kartus et al in 1999 noted that 33.6% of
604 patients after ACL reconstruction using the Patellar Tendon continued to suffer
from Anterior Knee Pain (159). Jarvela et al noted that only 40 of 91 patients
operated for ACL reconstruction using the Patellar Tendon were free of pain 7 years
later (160), though non had severe Patello-Femoral pain.
Meniscal Injury:

Meniscal injury imitating anterior knee pain syndrome should be excluded (122) as
it has been claimed to be present in up to 25% of cases (55). It is our experience
that a high degree of overlap exists between the lateral compartment of the knee
and the patello-femoral joint as it is not unusual that PFJ arthritis, especially of the
groove, is determined when clinically a lateral meniscus tear was suspected and
often a lateral meniscus tear is eventually found when arthroscopy is performed for
long standing diagnosed anterior knee pain syndrome.

Bone Scan and its relation to Stress Fracture, RSD and intra-osseous
pressure:
The bone scan has been shown to be positive in nearly half the cases of anterior
knee pain syndrome (25,26,27,28,29,257). This may represent a sympathetic
cause of knee pain as RSD (138,139,140,141,142,143,222,223,224,225) (Fig 2),
focal arthritic change (161), physiological reaction to blunt trauma (257) or
possibly trabecular stress fractures which may heal or may lead to subchondral
bone sclerosis and late cartilage degeneration (132). The intensity of uptake on
the bone scan may represent the severity and thus also the extent of the healing
process of the patello-femoral joint (31,257). The findings on a bone scan may be
also related to excessive blood supply to the diseased PFJ as seen by
thermography (225) or estimated by measuring the intra patellar pressure (32,33,
34) by direct measure or by phlebography (32,162).
Fig 3: Bipartite patella in a teenager: AP and lateral views
A. Anterior-Posterior view
B. Lateral view
C: Axial view (Skyline view)
D: Magnetic Resonance Imaging

This intra osseous pressure has been described as a cause of pain in osteoarthritis
(35,36,37,38,39,40,41,42) though delayed emptying of the venous compartment
of the painful patella was not demonstrated by Hominga in 1995 (162).

The intra osseous patellar pressure as a cause of AKP was further investigated by
Schneider in 2000 (271) and by Miltner in adolescents in 2003 (270). Schneider
demonstrated 90% success in 50 knees (40 patients) by extra articular drilling
when high intra-osseal pressure was demonstrated (271). Miltner showed good
results in adolescents using the same drilling technique (270).
Patello-Femoral Alignment:

Malalignment has been defined by Post, Teitge and Amis in 2002 (262) as follows:
"… bony alignment, joint geometry, soft tissue restraints, neuromuscular control
and functional demands, combine to produce symptoms as result of abnormally
directed loads which exceed the physiological threshold of the tissues".

Since the description of "malignant malalignment described by Brody in 1982,


including a wide pelvis, anteversion of the femur, valgus knees, external rotation of
the tibia and pronation of the feet (11,12,13) many varieties of malalignment have
been described: patella alta (high patella) (13,18,19,78,79,80) (Fig 4), increased Q
Angle (180), patella baja (low patella, usually hyathrogenic following surgery) (20,
73,103), which in itself could cause Osgood Schlatters disease or possibly Sindig-
Larsen-Johansen's Disease due to excessive force exerted on the patellar ligament
(73,74) (Fig 5 & Fig 6), a wide patella (72,308), leg length discrepancy (21,22,23,
24), flat feet which could be observed in 43% of patients suffering from anterior
knee pain syndrome as shown by Stanish in 1988 (15), foot pronation as shown by
Kessler and Darlene in 1983 (13), tight ileo tibial band (13), "squinting patella"
with a high Q-Angle (QA) (169) or lateralization of the patella for any reason (131,
133,137), on passive flexion or on active extension, as demonstrated by Witonski
and Goraj in 1999 (264). Lateralization of the patella could be demonstrated by x-
ray (63,82,83) (Fig 1), on a computerized tomogram or by MRI (17,25,64,131,
137,171,178,195,260). Sanchis-Alfonso & Rosello Sastre debated in 1999 the
possibility that malalignment would cause soft tissue damage and bring on pain
through neural over-growth and irritation (265). Duffey in 2000 demonstrated in
70 long distance runners the dynamic malalignment as a cause of AKP, inclusive of
low pronation at the initiation of the stance and High Arch, alongside Low
Extension Peak Torque and frequent change of running shoes (246). Hetsroni et al
(272) presented in 2006 a prospective study on 473 young adults before their
recruitment to army service at the age of 18, in whom dynamic pronation was
measured on walking on a Tread Mill, barefoot, at 5 Km/hr. No relation was found
between the various measures of pronation and the later development of AKPS
during their basic training.
Fulkerson & Arendt in 1999 and in 2000 (266,267) suggested in females that AKP
may be caused by the wide pelvis, lateral thrust on walking or running along side
sitting with legs together and using high healed shoes. Metin-Cubuk in 2000 (261)
suggested laterally placed Tibial Tuberosity as a cause of AKP (261), though he
found no relation to patellar height. In these cases transfer of the Tibial Tuberosity
could be considered. .Isolated femoral anteversion (168) or external rotation of the
tibia (171,172) could be corrected by tibial or femoral rotational osteotomy (171,
172) which may be a rather major surgical intervention for the discussed syndrome
as it cannot be overemphasized that virtually all the malalignments discussed have
been often debated as having any significant effect at all on the anterior knee pain
syndrome (19,86,109,116,230, 233,268,269) not excluding debates on the role of
the Q angle (176,263), patellar tilt (177) (Fig 1) and patella height (168,261) (Fig
4).

Moller and his coworkers published in 1989 a paper which surgeons dealing with
the patello-femoral joint should keep in mind (57): The author performed a Tibial
Tuberosity Transfer (TTT) in rabbits, and demonstrated 100% future occurrence of
microscopic degenerative changes in the joint cartilage with 50% showing overt
arthritic changes. Performing a TTT in an AKPS patient should not be undertaken
lightly.

Joint Laxity:

Joint laxity could possibly cause general joint pain (16), anterior knee pain
syndrome (81,86,245), possibly patellar dislocation (14,15) or even osteoarthritis
(17). Kujala et al in 1986 have shown a relation between anterior knee pain
syndrome and all measures presented in joint laxity namely drawer, knee
hyperextension and mediolateral mobility of the patella (86). Outerbridge and
Dunlop in 1975 suggested the relation between patellar instability and continued
Anterior Knee Pain (254).
Forces and Cartilage Degeneration of the Patello-Femoral Joint:

The extensor mechanism of the knee, working eccentrically absorbs 42% of the
actively absorbed energy of running at ground contact (180), with a moment five
times as strong in running than in walking (124). The force exerted in squatting to
the patello-femoral joint may reach 500 kg or x 6.5 body weight (1,2,173). On
jumping the forces may reach momentarily four times this measure (1) or 20 body
weight (66,173). The forces may be somewhat higher in a higher or lower than
normal Q angle (2). The forces on the patello-femoral joint of the unloaded or
loaded knee are appreciably higher on full horizontal extension than in flexion (3,
68,84) and the forces in women are higher because of a shorter patellar tendon
(4). Step climbing exerts three times body weight on the patello-femoral joint (65)
or far more in specific situations (66) as a combination of force and of the reduced
area of the patello-femoral joint on flexion (59).

Fig 6: Sindig-Larsen-Johansen Disease: note the heterotrophic calcification on the


lower pole of the patella.
Fig 7: Habitual dislocation of the left patella in a teenage girl.

Cartilage degeneration has been mentioned above as a possible cause of anterior


knee pain syndrome. This has been attributed to loss of proteoglycan from the
cartilage matrix (149) causing softening and eventual break down of the cartilage
and sub-chondral bone sclerosis causing loss of shock absorption and eventual
cartilage degeneration of the patellar surface (132) or overt degeneration of the
groove (147), differed from degeneration of the cartilage over the patella.

Though cartilage softening or degeneration has been claimed to arise from


excessive stress (95,131,133) no damage was noted even over 120,000 cycles
when pressures did not exceed 250-500 psi (95). Most authorities note lack of
use to cause softening and eventual degeneration of the articular cartilage (30,53,
54,110,183,191,192,221,253). Seedholm has shown softening of the PFJ cartilage
in areas not involved in daily activity (181,182) an observation obviating the
necessity for continuous life long physical activity, though continuous and not
traumatic in nature. This view, concerning the joints preservation effect offered by
dynamic continuous activity, is generally accepted by various authorities (185,186,
187,188,189,190) and as the subject of "running and osteoarthrities" is discussed
in detail else where we shall refrain from further discussion on this matter.

In dogs running uphill 4 Km a day the thickness of the uncalcified cartilage


increased 3-23% and the proteoglycan content increased up to 59% (192), giving
a stiffer articular cartilage. In dogs running 20 to 40 Km a day bone formation was
increased, trabecular bone volume was increased in the patello-femoral area, the
cartilage thickness and proteoglycan content increased in both aspects of the
patello-femoral joint, though loss of proteoglycan and mild cartilage softening was
noticed in the lateral femuro-tibial compartment (192) possibly due to acute over-
training.

Mori et al in 1991 (125) pointed out three groups of adolescents suffering from
Anterior Knee Pain. Working with 83 patients (98 knees) he described the AKPS
group, the Idiopathic Chondropathy group and the group of Unstable Patella. He
pointed out that the condition tends not to advance, and the damaged cartilage
would tend to heal. Price in 2000 (256) demonstrated that healing occurred in 4%
only, while 68% continued to suffer moderate to severe pain in 46 patients who
suffered direct patellar trauma. Mild patellar subluxation as a cause of AKP or
cartilage damage in female adolescents was also pointed out by Outerbridge &
Dunlop in 1975 (254).

Goodfellow et al in 1976 pointed out the appearance of surface degeneration


because of lack of use (253). They also noted Basal Degeneration of the deep
cartilage Layers, painful, and liable to surgical excision. Lack of use as causing
cartilage degeneration has been widely discussed by others as mentioned above
(30,53,54,110,181,182,183,191,192,221).

Joensen et al in 2001 (255) claimed chondral patellar damage to be located by MRI


in 17 of 24 athletes suffering AKP as opposed to similar findings in only 4 of 17
controls. Sensitivity of MRI in diagnosis of patellar cartilage damage, though with
low specificity, was shown by Lee in 2001 (258) and better accuracy using the
SPIR view of MRI was pointed out by Marcarini in 2004 (259).

In 1936 Owra (5) described the surprisingly high occurrence of macroscopic


cartilage changes on the patellar surface. These observations were later repeated
(6,7,8). Observations have shown changes on the cartilage surface to be apparent
in cadavers as early as the age of 10 (5,6) described in up to 85% of cadavers in
the 3rd decade and up to 100% in the 7th decade (8). The changes could often be
considered normal especially as even advanced cases may not show any clinical
symptoms (109,193) and the general relation between pain, macroscopic cartilage
damage and roengenographic appearance seems to questionable at the best (194).
In symptomatic patients about half will show no cartilage damage and vice versa
approximately half of asymptomatic patients may show cartilage damage (85,109).

Surgical Interventions merit a few words concerning their relation to the


observations discussed above. Cadaver studies have failed to show a lower PF
contact area when chondromalacia occurs (59). The same authors failed to show a
reduction of the patello-femoral joint pressure when a lateral release was
performed (59). Even though in joints with subluxing patella the contact of the
medial facet of the patella to the femur occurred in a more flexed angle of the knee
no difference was noted between normal and subluxing cadaver joints concerning
the occurrence of the medial facet chondro-malacia (87).

In general there is misclarity concerning the relation between the existence and
location of cartilage damage at the patelo-femoral joint to the success or failure of
surgical procedures devised for anterior knee pain syndrome (56). The success of
the Insall procedure (lateral release, medial plication and vastus medialis
advancement) has been reported to stand in correlation with the congruence angle
and to the grade of chondromalacia (88,89,90). Another element related to the
success of lateral and more so of medial arthrotomies is the denervation caused by
the procedure to the patello-femoral joint (96,97,98,100,101,102).

Grading Cartilage Damage:


The grades of cartilage damage or chondromalacia were outlined by Outerbridge in
1961 (9). He described four grades of cartilage degeneration:
1. Softening
2. Fibrillation
3. Cracking or partial thickness damage
4. Exposed bone
Ahlbach in 1968 (10) graded the roentgenological appearance to six grades:
1. narrowing
2. Loss of joint space
3. Slight bone defect
4. Moderate bone defect
5. Severe bone defect
6. Joint Subluxation

The Ahlbach classification has little to do with anterior knee pain syndrome and its
obvious that outerbridge grade I, II and even III will not even show up on
roentgenographic evaluation and may be shown occasionally only on MRI (126,
196,197,255,258,259).

Two questions must be presented in conclusion of this section:


1. Does the injured cartilage regenerate?
Cartilage has the ability to thicken in the human patella (104) or in
experimental animals (192). It has also a certain, though limited, ability to
heal and regenerate (105,106,107,108,109,114). This ability, though limited,
is seen more in full thickness cartilage defects (202) and may be assisted by
passive motion (202). Mori et al in 1991 reported macroscopic healing of
malacic cartilage of the patella (125) of 98 adolescent knees in 83 patients
suffering from AKPS.
2. Does anterior knee pain syndrome lead to osteoarthritis?
Bently, Meachin and their co-authors claimed in 1977, 1984 and 1985 that
only the 3% chondromalacia patients affecting the lateral facet may lead to
overt osteoarthitis while 97% affecting the medial facet do not (105,109,113).
Similar findings were noted by Eckstein et al in 1993 (252) claiming the medial
patellar cartilage lesions to be located over less calcified bone and not to
progress. In other words no more than 3% of cartilage lesions in AKP patients
will progress to osteoarthritis. Karlson back in 1940 claimed that no
osteoarthritis developed in these patients after 20 years follow up (112).
Patellar Dislocation:

Patellar dislocation (Fig 7) is out of the scope of this paper and will be discussed
only briefly, as patellar Subluxation (254) and dislocation are recognized as causes
of AKP.

Joint laxity seems to comprise a risk factor (14) and a low sulcus angle as seen on
CT or MRI will predispose to this condition (64). The general measurements
concur to those in patellar subluxation (19), though arthritic changes seem to be
more prevalent in patellar dislocation. Arthroscopy will show contact of the patellar
ridge and the medial facet at deeper flexion than

Fig 4: Patellar height in AP and lateral views:


Lateral views (note Osgood-Schlatter disease)
A. High positioned Patella B. Normal positioned Patella
Fig 4: Patellar height in AP and lateral views: Anterior-Posterior views
C. High positioned Patella D. Normal positioned Patella

Fig 5: Osgood Schlatter Disease A-B:note the heterotrophic calcification over and
proximal to the tibial tuberosity.

in anterior knee pain syndrome patients (87). In acute dislocation some advocate
immediate surgery (201) though even then a 17% reoccurrence rate has been
reported (201). It seems that treatment of acute dislocation should be
conservative (93) and no advantage has been shown using a cylinder cast when
compared to a simple elastic bandage (94).
Psychological Factors in AKPS:

In 1982 Mr. Nordon Trickey of the Royal National Orthopaedic Hospital in


Stanmore, London, was requested to speak of Anterior Knee Pain in the
Arthroscopy course of Cambridge. Many remember his opening words when he
said: "To ask an Orthopaedic Surgeon to speak on Anterior Knee Pain is like asking
a Psychiatrist to speak on Gun-Shot wounds of the abdomen".

Thomee et al in 2002 noted that AKPS patients score high on the "catastrophizing
scale" (274) and Fulkerson in 2004 (230) pointed out the necessity to identify any
hysterical tendency in these patients.

Witonski in 1999 (275) pointed out the possibility of AKPS existing as a


psychosomatic disease with only sub-clinical patellar instability and little, if any,
relation to physical activity.

Dr. Jack Andrish allowed us to mention their Research in Cleveland concerning


Chronic Pain in children inclusive of AKPS as presented recently at the
International Patello-Femoral Study Group Meeting and at the Rocky Mountain
Trauma Society. He showed 30.7% of the children to have suffered some sort of
psychological trauma, with 12.5% of the children suffering chronic pain disclosing a
story of sexual abuse.

It is interesting to note the study of Witvrouw et al in 2000 (245), whom in a


prospective study in 282 young adults aged 18.6 years in average, found no
correlation between the occurrence of AKPS and a psychological test performed
prior to the AKP occurrence.

The Concept of Core Stability:

The term "Core Stability" is more popular among Physical Therapists and Athletic
Trainers than among Physicians (277). As described by Wilson in 2005 (277) the
"Core" is composed of the Lumbar Vertebrae, the Pelvis, the Hip joints, and the
active and passive structures that either produce or restrict movement of these
segments. The "Core" would probably affect Lower and Upper Limb function, Trunk
function and Pain Syndromes, and may not yet be fully understood.

Sutter et al in 1999 described the change in the Quadriceps Muscle reaction after
Sacro-Ileac or spine manipulation in AKPS patients (278) and raised the question
whether similar maneuvers would affect AKPS. Baker et al in 2002 pointed out the
deficient Proprioception in AKPS (279), though this would not necessarily be
related to Core Stability. Ireland and Wilson in 2003 (280) in females aged 12 to
21 and suffering from AKPS showed a reduction of 26% in peak hip abduction force
and a reduction of 36% in peak hip external rotation force. Zhang et al in 2000
(281) showed the hip extensor muscles to absorb 25% of the landing impact, and
thus deficient hip extensors would over load the knee, possibly enhancing the
occurrence of AKPS.

Measurements in Anterior Knee Pain Syndrome:

Various authors have attempted to correlate certain clinical and roentgenographic


measurements with pain or subluxation of the patello-femoral joint (19). These
include the Q-Angle in extension (120) or flexion (the tubercle-sulcus angle)(121),
the patellar height estimated by the Insall-Salveti index (60)or Blackboure index
(61) (Fig 4), the sulcus or congruence angle according to Merchant (63) and
Laurin's sulcus measurements (63,82,83,98,228). The various groove
measurements are probably best achieved by computerized tomography or MRI
(25,64,137,170,178,195,260). All measurements have been correlated to
occurrence of anterior knee pain or patellar subluxation (13,18,19,77,78,79,80)
(Fig 1).

Physical Examination:

Along side a full medical history concerning the knee a full standardized knee
examination should be undertaken (227). This would include swelling, sensitivity,
range of motion, stability, meniscal tests and examination of the patello-femoral
joint. Examination of the patello-femoral joint should include the longitudinal
compression test performed by applying firm pressure on the patella as the knee is
actively extended from a moderately flexed position and the transverse friction
test. These should never be done in full extension as the synovium will be pinched
under the patella causing acute pain. Both lateral and medial articular surfaces of
the patella should be palpated and the upper and lower poles for quadriceps or
patellar tendon disease (Fig 5 & Fig 6). Attention should be directed to the supero-
lateral aspect of the patella in an attempt to diagnose a bipartite patella (Fig 3).
Lateral tilting of the patella should be performed while checking for a tight lateral
retinaculum (120,121,221) (Fig 1). Normally when lifting the lateral border of the
patella with the knee extended, the lateral edge of the patella should achieve a
horizontal or over horizontal position (122). The patello-femoral tracking should
be assessed (122) and the patella and limb alignment evaluated. Patellar glide
should be performed (122) by shifting the patella to lateral. We estimate the
patellar stability by dividing the patella to quadrants: gliding of the patella up to
one quadrant would mean the patella is hypo-mobile, one to two quadrants is
normal, two to three quadrants is slightly hyper-mobile, three to four quadrants is
moderately hyper-mobile and when the whole patella may be shifted out of the
groove the patella is severely hyper-mobile. This examination should be
completed by performing the apprehension test when the patient is requested to
flex his knee while the patella is shifted laterally. If the patient tends to dislocate
his patella he will be apprehensive to flex his knee feeling the patella may dislocate
(227). Eventually, quadriceps tightness should be checked (122) and leg length
discrepancy excluded. Good correlation between patients complaints and physical
examination has been reported (123).

Natural Course and Treatment:

Natural Course of the Disease:


The natural course of anterior knee pain syndrome is not always predictable and its
course may be treacherous and frustrating both to the doctor and to the patient.
Though arthritic changes generally do not develop as previously discussed (109)
Anterior Knee Pain Syndrome may not always yield to conservative treatment and
often it may seem that far more than 10% may need further intervention. Older
patients may react unfavorably to any type of treatment, conservative or surgical
(206). Presence of anatomic cartilage softening may prevent conservative therapy
to alleviate the symptoms (134) and possibly also malalignment caused by a
"squinting patella" (172). 3.5% of recruits were reported by Wilson in 1983 to
have been released from the service because of anterior knee pain syndrome (205)
and lack of improvement in 35% of over use injuries with only 37% totally healed
was reported by Almekinders twice in 1994 (206,213). The author remarked that
the worst of these were the anterior knee pain syndrome patients (206,213).
Conservative treatment has been reported to be successful in 34% of patients
only, as has been reported by Eden in army personnel in 1992 (211) and a 66%
failure rate was reported by Quaile in 1969 (212).

Others claim relatively good results with 90% success with conservative therapy
(122) and spontaneous healing especially in the younger patient has been reported
by Cascells in 1982 (207). Whitelaw in 1989 (208) reported successful treatment
in 87%, 68% of these staying permanently well. Over 80% success of conservative
therapy was also reported by Ruffin in 1993 (209) and by Jensen & Albrektsen in
1990 (210) who specifically warned of unessential surgical procedures (210).

Conservative Treatment:
Treatment of anterior knee pain syndrome is conservative. Conservative treatment
will suffice in 90% of patients (122). This would include activity modification, non
steroid anti-inflammatories, stretching, strengthening, endurance training and
agility (122). A course of taping accompanied by muscle training and
maintenance, possibly assisted by EM6 and biofeedback, is often helpful (203). A
soft knee brace may affect the position of the patella as determined by the "Sulcus
Angle" (292) and is often useful both in treatment and in prevention (119,282). We
find a custom made insole is often of major assistance (219). In certain situations
a simple silicon rubber heel cushion may have a positive preventive effect on the
occurrence of anterior knee pain syndrome (118). Conservative treatment should
continue for 3-12 months (122) before arthroscopy or further surgical intervention
is advised.

A relatively large amount of research has been directed to various modalities of


treatment for AKPS. Doucett and Goble in 1992 (283) using strengthening and
stretching of the Quadriceps showed an 84% improvement over eight weeks.
Kannus et al in 1999 (284) using Quadriceps strengthening, rest and NSA
medication showed 75% of patients to still be free of pain 6 months to 7 years
after treatment. Bennett & Stauber in 1986 (285) showed Eccentric Quadriceps
Torque to be reduced in 41 of 130 patients suffering from AKPS and these
improved following two to four week of Eccentric Training using an Isokinetic
Dynamometer. Roush et al in 2000 (290) demonstrated improvement in AKPS
patients in a blind and controlled trial using the MUNCIE method to strengthen the
Vastus Medialis Muscle. Lam and Ng in 2001 (286) advised using EMG for
effectively strengthening the Vastus Medialis Muscle in variable positions. Herbert
in 2001 (287) demonstrated the superiority of strengthening exercise over taping,
as was also shown by Clark et al in 2000 (291), who in a randomized and
controlled trial showed improvement by stretching and strengthening, but not by
taping. As opposed to these findings Powers in 1997 (288) and Cowan in 2002
(289) showed the positive effect of taping both on pain as on the Vastus Medialis
versus Vastus Lateralis firing sequence, according to the works of MacConnell in
1986 (203). The technique of taping could be claimed to account for the failure or
success of this method.

Stretching especially of the Quadriceps, would probably reduce AKP following three
months of treatment (233). Reduced Quadriceps and Gastrochemius Flexibility has
been shown as a causative factor in AKPS by Witvrouw in 2000 (245) and Hartig
and Henderson in 1999 (293) showed the effect of Hamstring stetching in
prevention of the disease in young military recruits.

A placebo controlled treatment course was held by Crossley et al in 2002 (294).


The treatment group received Taping, Quadriceps strengthening, biofeedback
assisted muscle training, Gluteal strengthening, and stretching the Quadriceps and
Hamstrings. Both the placebo treated group and the research group improved,
though the treatment group improved significantly more.

In 1996 Dye proposed the concept of "The Envelope of Function". The concept was
described as the "Range of load that can be applied across an individual joint in a
given period without Supra-physiologic overload or structural failure". AKPS could
be treated by reducing patient activity to within the Envelope of Function and
gradually extending the Envelope by gradual strengthening, stretching and training
(307).

Surgical Treatment:
Surgery in anterior knee pain should be reserved for the most exceptional cases
and then kept to the minimum possible and directed to specific and clear
pathology. Extreme caution should be used when deciding on surgical means
(210) and most so when symptoms are vague and especially when bilateral. In
well selected cases, success of surgery may reach 80% (214) but as many of us
know from experience every major hospital has one or two total disasters.

Surgical procedures are mostly designed to improve alignment: lateral retinacular


release, the Insall procedure, tibial rotation osteotomy or tibial tuberosity transfer.
The first two are proximal realignment procedures consisting of soft tissue
manipulation and the second two are distal bony procedures. Lateral retinacular
release may be used for releasing excessive lateral pressure or lateral retinacular
tightness. Shea and Fulkerson in 1992 (305) showed a 92% success rate when
patellar tilt was evident and cartilage lesions not severe. Post in 2005 (233)
warned against severe failures, while Fulkerson in 2002 (306) drew attention to
pain originating from iatrogenic Medial Patellar Subluxation. Tibial tuberosity
transfer may be used for relieving excessive patello-femoral pressure by elevating
the tibial tuberosity. Late complications of this procedure should be kept in mind,
especially secondary arthrosis as discussed earlier in this text (57). Patelectomy
has been used in persistent cases, occasionally with good results (215,217), and
thinning of the patella aimed to reduce patello-femoral pressure has been
described (216). Patella drilling or osteotomy has been devised in order to reduce
intra osseous pressure (218,270,271).

When cartilage damage to the patella has been unequivocally demonstrated,


surgical debriedment would offer moderate results (295), possibly better using
Bipolar Radiofrequency (296) though use of radiofrequency may lead to
detrimental future negative effects on bone and cartilage (297). In more severe
damage Micro-Fracture or Abrasion Chondroplasty exposing the sub-chondral bone
and letting access to the joint surface of bone marrow cells would be the next line
of treatment (304), while autologous cartilage cell implantation (ACI) (299,300,
301,302,303) with or without realignment (233) would be reserved as the last
cause of treatment.

Further details on the surgical procedures are beyond the scope of this manuscript.

Prevention:

There is little known about prevention of anterior knee pain syndrome. Previous
research in our unit seems to indicate prevention is possible or at least enables
some reduction in the severity of the disease. The first research project utilized a
silicon shock absorbing heel in the police anti-terrorist unit where anterior knee
pain syndrome reached 50% occurrence (118). 15 fighters were given a silicon
heel in training and 40 continued training without the heel. 20 of the 40
complained of anterior knee pain during the course while only 2 of the 15 who used
the heel complained of this problem. This finding was significant (p=0.013). In
the study we did not differentiate anterior knee pain syndrome from patellar
tendinitis (Jompur's knee). In a second study we used a custom made insole in
100 police recruits while 100 continued training with the standard military boot.
24% suffered from Anterior Knee Pain Syndrome using their unmodified boot while
18% suffered anterior knee pain syndrome using the insole. When comprising an
"injury score" based on multiple pathology sights and severity we found a score of
96 in the group using the military boot and a score of 56 in those who had the
insole added in the same shoe (219). In a further study in the same group, we
supplied 50 recruits with a specially designed shoe with a flexible shock absorbing
and supportive sole and a snug fitting upper ("A-T 100", built by New Balance to
specified request). In this group 10.5% only complained of anterior knee pain as
opposed to 24% using the standard military boot and the "injury score" was 39
compared to 96 (219). In a third study conducted with the Army Center of
Physical Education 81 men and women due to start an intensive course were
randomly divided into two groups, one of which was supplied with a knee brace for
all activities while the other was not given a knee support unless medically
requested for other reasons. 57% of the group not using the brace developed
Anterior Knee Pain Syndrome during the course while only 15% of the brace group
developed similar complaints. This was slightly more emphasized in the women.
The results were statistically significant (p<0001) (111,119).

Van Tiggelen et al repeated this trial in the Belgian Army in 2004 (282). In 167
military recruits, 18.5% developed AKP during their basic training as opposed to
37% of the control group.

Hartig & Henderson in 1999 (293) in 150 military recruits and 148 controls showed
reduction of the occurrence of over use injuries inclusive of AKPS using a
Hamstrings stretching program. Witvrouw in 2000 (245) in a prospective study
inclusive of 282 young adults aged 18.6 years in average, showed again the
importance of Quadriceps and Gastrochemius flexibility. On the other hand, though
stretching is widely prescribed in order to prevent over use injuries (309), the
preventive role of stretching may not be proven (310), or may even be associated
with injured cohorts (311). Nevertheless, until shown otherwise, stretching should
probably be practiced as part of the preventive program in reducing the occurrence
of AKPS (246). Dye in 1996 (307) discussed, as mentioned above, the importance
of remaining within "the Envelope of Function", which would be gradually extended
though progressive training.

In summary, it may be concluded that prevention of anterior knee pain syndrome


may be possible by the preventative use of a heel shock absorber, good custom
made insoles, well designed shoes and a knee brace, along side good muscle
power and flexibility, developing proprioceptive ability and keeping within the
expanding limits of the "Envelope Of Function".

Summary:

We have discussed various aspects and controversies of Anterior Knee Pain


Syndrome, especially in adolescents, including occurrence, anatomy, etiology,
pathology, differential diagnosis, roentgenology, conservative and surgical
treatments. We have specified the physical examination and dealt with the
question of cartilage degeneration, the natural history of the disease, prevention
and prognosis.

In order to assist in decision making in this complex entity, Kelly and his associates
devised in 1998 an algorithm for diagnosis, conservative and surgical treatment
(122). This algorithm seems to be a useful tool to assist the surgeon in decision
making and possibly reduce the incidence of unnecessary errors, mistakes and
over zealous unnecessary treatment.

REFERENCES

1. Hess, Hoberty. Sports Injuries. Williams & Wilkins, 1985.


2. Huberti HH, Hayes WC. Patellofemoral contact pressures. The influence of q-angle and tendofemoral
contact. J Bone Joint Surg 1984 Jun;66(5):715-24.
3. Grood ES, Suntay WJ, Noyes FR, Butler DL. Biomechanics of the knee-extension exercise. Effect of
cutting the anterior cruciate ligament. J Bone Joint Surg 1984;66(5):725-34
4. Nisell R. Mechanics of the knee. A study of joint and muscle load with clinical applications. Acta
Orthop Scand Suppl 1985;216:1-42.
5. Owra AA. Chondromalacia Patella. Acta Chir Sc. 1936;77:Suppl. 41. .
6. Radin EL. Anterior Knee Pain: The need for a specific diagnosis, stop calling it chodromalacia! Orthop
Rev 1985;14:128-134.
7. Boe S, Hansen H. Arthroscopic partial meniscectomy in patients aged over 50. J Bone Joint Surg
1986;68(5):707.
8. Sideman, Wolin, et al. Surg Clin N.A. 1949;29:261-67.
9. Outbridge. J Bone Joint Surg 1961;43B:752.
10. Lysholm J, Hamberg P, Gillquist J. The correlation between osteoarthrosis as seen on radiographs
and on arthroscopy. Arthroscopy 1987;3(3):161-5.
11. Brody DM. Techniques in the evaluation and treatment of the injured runner. Orthop Clin North Am
1982;13(3):541-58.
12. Landry ME, Zebas C. Analysis of 100 knees in high school runners. J Am Podiatr Med Assoc
1985;75(7):382-4.
13. Kessler, Darlene. Management of Common Musculoskeletal Disorders. Harper & Row, 1983.
14. Eleinbreck, Springorum HW. Orthop. Three Grezgd 1984;118:751-60 in Ex. Med. Ortho Sec.
1982;33:Abs 881.
15. Stanish WD. ESKA Meeting. 1986
16. Finsterbush A, Pogrund. The hypermobility syndrome. Musculoskeletal complaints in 100
consecutive cases of generalized joint hypermobility. Clin Orthop 1982;(168):124-7.
17. Shapiro, Nahir, Sharef. The hypermobility syndrome. Harefuah 1984;106:270-72.
18. Carson WG Jr, James SL, Larson RL, Singer KM, Winternitz WW. Patellofemoral disorders: physical
and radiographic evaluation. Part II: Radiographic examination. Clin Orthop 1984;(185):178-86.
19. Aglietti P, Insall JN, Cerulli G. Patellar pain and incongruence. I: Measurements of incongruence.
Clin Orthop 1983;(176):217-24.
20. Marshall DJ. AJSA 1984;17:727-8.
21. Temple C. Sports injuries. Hazards of jogging and marathon running. Br J Hosp Med
1983;29(3):237-9.
22. Friberg. Leg length asymmetry in stress fractures. A clinical and radiological study. J Sports Med
1982;22:485-8.
23. Friberg O. Clinical symptoms and biomechanics of lumbar spine and hip joint in leg length
inequality. Spine 1983;8(6):643-51.
24. Gross RH. Leg length discrepancy in marathon runners. Am J Sports Med 1983 May-Jun;11(3):121-
4.
25. Bentley G, Dowd G. Current concepts of etiology and treatment of chondromalacia patellae. Clin
Orthop 1984;(189):209-28.
26. Lin D, Alavi A, Dalinka M. Bone scan evaluation of patellar activity. Int J Nucl Med Biol
1981;8(1):105-9.
27. Dye SF, Boll DA. Proceedings Int. Knee Soc, Am J Sports Med 1985;13:432.
28. Dye SF, Boll DA. Radionuclide imaging of the patellofemoral joint in young adults with anterior knee
pain. Orthop Clin North Am 1986;17(2):249-62..
29. Perugia P. Lecture, June 1980, Rome.
30. Kahanovitz N, Bullough P, Jacobs RR. The effect of internal fixation without arthrodesis on human
facet joint cartilage. Clin Orthop 1984 Oct;(189):204-8.
31. Dye SF, Proceedings Int. Knee Soc. In: Am J Sports Med 1989;17:727.
32. Heigaard, Hortelius. Acta Orthop Scand 1983;54:779-81.
33. Hejgaard N, Arnoldi CC. Osteotomy of the patella in the patellofemoral pain syndrome. The
significance of increased intraosseous pressure during sustained knee flexion. Int Orthop
1984;8(3):189-94.
34. Hejgaard N, Larsen E. Value of early attention to spinal compression syndromes. Acta Orthop Scand
1984;55(2):234-7.
35. Arnoldi CC, Linderholm H, Mussbichler H. Venous engorgement and intraosseous hypertension in
osteoarthritis of the hip. J Bone Joint Surg [Br] 1972;54(3):409-21.
36. Phillips RS, Bulmer JH, Hoyle G, Davies W. Venous drainage in osteoarthritis of the hip. A study
after osteotomy. J Bone Joint Surg [Br] 1967;49(2):301-9.
37. Phillips RS. Phlebography in osteoarthritis of the hip. J Bone Joint Surg [Br] 1966;48(2):280-8.
38. Arnoldi CC, Lemperg R, Linderholm H. Immediate effect of osteotomy on the intramedullary
pressure in the femoral head and neck in patients with degenerative osteoarthritis. Acta Orthop Scand
1971;42(5):454-5.
39. Arnoldi CC, Lemperg K, Linderholm H. Intraosseous hypertension and pain in the knee. J Bone Joint
Surg [Br] 1975 ;57(3):360-3.
40. Lenperg, Arnotti. Clin Ortho 1978;130:143-56.
41. Finestone A, Radin E, Lev B et al. Treatment of overuse patellofemoral pain. Prospective
randomized clinical trial in a military setting, Clin Orthop 1993;193:208-210.
42. Richard, Lonergan. Orthopedics 1984;7:1705-7.
43. Fulkerson JP, Tennant R, Jaivin JS, Grunnet M. Histologic evidence of retinacular nerve injury
associated with patellofemoral malalignment. Clin Orthop 1985;(197):196-205..
44. Fulkerson JP. The etiology of patellofemoral pain in young, active patients: a prospective study. Clin
Orthop 1983;(179):129-33.
45. Krompinger WJ, Fulkerson JP. Lateral retinacular release for intractable lateral retinacular pain. Clin
Orthop 1983;(179):191-3.
46. Ficat P, Masson CIE. The role of articular cartilage in patellofemoral pain. Orthop Clin North Am
1986 Apr;17(2):231-4.
47. Insall J. Current Concepts Review: patellar pain. J Bone Joint Surg [Am] 1982;64(1):147-52.
48. Fulkerson JP, Tennant R, Jaivin JS, Grunnet M. Histologic evidence of retinacular nerve injury
associated with patellofemoral malalignment. Clin Orthop 1985;(197):196-205
49. Chrisman OD. The role of articular cartilage in patellofemoral pain. Orthop Clin North Am
1986;17(2):231-4.
50. Nangle. J Bone Joint Surg 1972;51B:382.
51. Elmer RM. Persistent congenital isolation of the suprapatellar pouch mimicking patellofemoral
disease. J Pediatr Orthop 1984;4(5):623-4.
52. Keene, et al. Proceedings Ortho Society, J Bone Joint Surg 1989;71B:879.
53. Goodfellow J, Hungerford DS, Zindel M. Patello-femoral joint mechanics and pathology. 1. Functional
anatomy of the patello-femoral joint. J Bone Joint Surg [Br] 1976;58(3):287-90.
54. Hehne HJ. Biomechanics of the patello-femoral joint and its clinical relevance, Clin Orthop
1990;258:73-85.
55. Fowler PJ, Lubliner JA. The predictive value of five clinical signs in the evaluation of meniscal
pathology. Arthroscopy 1989;5(3):184-6.
56. Christensen F, Soballe K, Snerum L. Treatment of chondromalacia patellae by lateral retinacular
release of the patella. Clin Orthop 1988;(234):145-7..
57. Moller BN, Moller-Larsen F, Frich LH. Chondromalacia induced by patellar subluxation in the rabbit.
Acta Orthop Scand 1989;60(2):188-91.
58. Smith AJ. A study of forces on the body in athletic events with particular reference to jumping,
Ph.D. Thesis, Leeds, England 1972.
59. Huberti HH, Hayes WC. Contact pressures in chondromalacia patellae and the effects of capsular
reconstructive procedures. Orthop Res 1988;6(4):499-508.
60. Insall J, Salvati E. Patella position in the normal knee joint, Radiology 1971;101:101-4.
61. Blackburne JS, Peel TE. A new method of measuring patellar height. J Bone Joint Surg [Br]
1977;59(2):241-2.
62. Laurin CA, Levesque HP, Dussault R, Labelle H, Peides JP. The abnormal lateral patellofemoral
angle: a diagnostic roentgenographic sign of recurrent patellar subluxation. J Bone Joint Surg [Am]
1978;60(1):55-60.
63. Merchant AC, Mercer RL, Jacobsen RH, Cool CR. Roentgenographic analysis of patellofemoral
congruence. J Bone Joint Surg [Am] 1974;56(7):1391-6.
64. Kujala UM, Osterman K, Kormano M, Nelimarkka O, Hurme M, Taimela S. Patellofemoral
relationships in recurrent patellar dislocation. J Bone Joint Surg [Br] 1989;71(5):788-92.
65. Leading Article, Br Med Journal 1981;1014.
66. Williams. MediSport 1980;2:22-25.
67. Olerud C, Berg P. The variation of the Q angle with different positions of the foot. Clin Orthop
1984;(191):162-5.
68. Nicholos, Hirshman. The Spine & Lower Limb in Sport. Mosby, 1986;718-20.
69. Dorell ST. Proceedings British Ortho Society Sep 88, J Bone Joint 1989;71B:875.
70. Martens M. Tendinitis of the patellar tendon. Acta Orthop Belg 1982 May-Jun;48(3):453-4.
71. Methany J, Mayor M. Am. J. Knee Surg. 1988;1:134-39 in Adv. Ortho surg 1988;12:134-35.
72. Harper et al. Proceedings British Knee Society Sep 88, J Bone Joint 1989;71B:886.
73. van Eijden TM, Kouwenhoven E, Weijs WA. Mechanics of the patellar articulation. Effects of patellar
ligament length studied with a mathematical model. Acta Orthop Scand 1987;58(5):560-6.
74. Lancourt JE, Cristini JA. Patella alta and patella infera. Their etiological role in patellar dislocation,
chondromalacia, and apophysitis of the tibial tubercle. J Bone Joint Surg 1975;57(8):1112-5.
75. Ferretti A, Puddu G, Mariani PP, Neri M. The natural history of jumper's knee. Patellar or quadriceps
tendonitis. Int Orthop 1985;8(4):239-42.
76. Jerosch JG, Castro WH, Jantea C. Stress fracture of the patella. Am J Sports Med 1989;17(4):579-
80.
77. Ficat, Hungerford. Disorders of the PFJ. Williams & Williams, 1977.
78. Insall J, Falvo KA, Wise DW. Chondromalacia patellae. A prospective study, J Bone Joint Surg 1976
Lancourt JE, Cristini JA. Patella alta and patella infera. Their etiological role in patellar dislocation,
chondromalacia, and apophysitis of the tibial tubercle. J Bone Joint Surg 1975;57(8):1112-5.
79. Lancourt JE, Cristini JA. Patella alta and patella infera. Their etiological role in patellar dislocation,
chondromalacia, and apophysitis of the tibial tubercle. J Bone Joint Surg [Am] 1975 Dec;57(8):1112-5.
80. Marks KE, Bentley G. Patella alta and chondromalacia. J Bone Joint Surg [Br] 1978;60(1):71-3.
81. Dandy DJ, Poirier H. Chondromalacia and the unstable patella. Acta Orthop Scand 1975;46(4):695-
9.
82. Carson WG Jr, James SL, Larson RL, Singer KM, Winternitz WW. Patellofemoral disorders: physical
and radiographic evaluation. Part I: Physical examination. Clin Orthop 1984;(185):165-77.
83. Carson WG Jr, James SL, Larson RL, Singer KM, Winternitz WW. Patellofemoral disorders: physical
and radiographic evaluation. Part II: Radiographic examination. Clin Orthop 1984;(185):178-86.
84. Hungerford DS, Lennox DW. Rehabilitation of the knee in disorders of the patellofemoral joint:
relevant biomechanics. Orthop Clin North Am 1983;14(2):397-402.
85. Dashefsky JH. Arthroscopic measurement of chondromalacia of patella cartilage using a
microminiature pressure transducer. Arthroscopy 1987;3(2):80-5.
86. Kujala UM, Osterman K, Kvist M, Aalto T, Friberg O. Factors predisposing to patellar chondropathy
and patellar apicitis in athletes. Int Orthop 1986;10(3):195-200.
87. Sojbjerg JO, Lauritzen J, Hvid I, Boe S. Arthroscopic determination of patellofemoral malalignment.
Clin Orthop 1987 Feb;(215):243-7.
88. Insall JN, Aglietti P, Tria AJ Jr. Patellar pain and incongruence. II: Clinical application. Clin Orthop
1983;(176):225-32.
89. Insall J, Falvo KA, Wise DW. Chondromalacia Patellae. A prospective study. J Bone Joint Surg [Am]
1976 Jan;58(1):1-8.
90. Insall J, Bullough PG, Burstein AH. Proximal "tube" realignment of the patella for chondromalacia
patellae. Clin Orthop 1979;(144):63-9.
91. Krahl H. 3rd International Jerusalem Symposium on Sports Medicine, Jerusalem, Jan 87.
92. Sachs RA, Daniel DM, Stone ML, Garfein RF. Patellofemoral problems after anterior cruciate
ligament reconstruction. Am J Sports Med 1989;17(6):760-5.
93. Larsen E, Lauridsen F. Conservative treatment of patellar dislocations. Influence of evident factors
on the tendency to redislocation and the therapeutic result. Clin Orthop 1982;(171):131-6.
94. Larsen E, Lauridsen F. Results of conservative treatment of patellar dislocations. Acta Orthop Belg
1982 May-Jun;48(3):455-62.
95. Zimmerman NB, Smith DG, Pottenger LA, Cooperman DR. Mechanical disruption of human patellar
cartilage by repetitive loading in vitro. Clin Orthop 1988;(229):302-7.
96. Abraham E, Washington E, Huang TL. Insall proximal realignment for disorders of the patella. Clin
Ortho 1989;248:61-65.
97. Moller BN, Helmig O. Patellar pain treated by neurotomy. Arch Orthop Trauma Surg
1984;103(2):137-9.
98. Laurin. Ortho Trans 1983;7:169-70.
99. Peterson L, Renström P. Sports Injuries, their prevention and treatment. Martin Dunitz, London,
1986; p. 303-305.
100. Arthornthurasook A, Gaew-Im K. Study of the infrapatellar nerve. Am J Sports Med
1988;16(1):57-9.
101. Baudet B, Durroux R, Gay R, Mansat M, Martinez C, Rajon JP.
[Patellar innervation. Surgical consequences]. [Article in French]. Rev Chir Orthop Reparatrice Appar
Mot 1982;68 Suppl 2:104-6.
102. Swanson AJ. The incidence of prepatellar neuropathy following medial meniscectomy. Clin Orthop
1983;(181):151-3.
103. Marshall. Proceedings or Soc. Oct 1987, J Bone Joint 1989;71B:105.
104. Van Hussen. Proceedings Neth O Soc 1985, Acta Ortho Scand 1985;56:449.
105. Bentley G. Articular cartilage changes in chondromalacia patellae. J Bone Joint Surg [Br]
1985;67(5):769-74.
106 Chrisman OD. The role of articular cartilage in patellofemoral pain. Orthop Clin North Am
1986;17(2):231-4.
107. Ohno O, Naito J, Iguchi T, Ishikawa H, Hirohata K, Cooke TD. An electron microscopic study of
early pathology in chondromalacia of the patella. J Bone Joint Surg [Am] 1988;70(6):883-99.
108. Willett KM, Simmons CD, Bentley G. The effect of suction drains after total hip replacement. J Bone
Joint Surg [Br] 1988;70(4):607-10.
109. Bentley G, Dowd G. Current concepts of etiology and treatment of chondromalacia patellae. Clin
Ortho Related Research 1984;(189):209-228.
110. Alexander CJ. Relationship between the utilisation profile of individual joints and their susceptibility
to primary osteoarthritis. Skeletal Radiol 1989;18(3):199-205.
111. Mann G, Ben Gal S, Finsterbush A, Frankel U, Matan Y. Anterior knee pain syndrome: prevention
by using a knee support with a patellar guiding ring. A prospective and randomized study, Proceedings
Congress International de Groupement Latin et Mediterraneen de Medecine du Sport, Montpellier, June
1993.
112. Karlson S. Chondromalacia patella. Acta Chir Scand 1940;83:347-381.
113. Meachim G, Bentley G, Baker R. Effect of age on thickness of adult patellar articular cartilage. Ann
Rheum Dis 1977;36(6):563-8.
114. Bentley G. The surgical treatment of chondromalacia patellae. J Bone Joint Surg [Br]
1978;60(1):74-81.
115. Fox J. Personal communication, Southern California Orthopaedic Institute, Los Angeles, 1994.
116. Fairbank JC, Pynsent PB, van Poortvliet JA, Phillips H. Mechanical factors in the incidence of knee
pain in adolescents and young adults. J Bone Joint Surg [Br] 1984;66(5):685-93.
117. Milgrom C, Finestone A, Eldad A, Shlamkovitch N. Patello-femoral pain caused by
over-activity: a prospective study of the effect of the appropriateness of foot-shoe fit and training shoe
type on the incidence of overuse injuries among military recruits, Milit Med 1992;157:489-490.
118. Mann G, Soran A, Borovski A, Matan Y, Sivan A, Yelinic Y, Simkin A, Yarom J, Frankl U, Finsterbush
A. Over-use injuries in an elite anti-terrorist fighting unit: relation to previous physical activity, relation
to anthrpometric, physimetric spirometric and ergometric performance, and effect of a silicon heel
shock absorber, Proceedings of the 5th Congress of ESKA, Palma de Mallorca, Spain, May 1992.
119. Mann G, Ben Gal S, Finsterbush A, Frankl U, Matan Y. Anterior knee pain syndrome: prevention by
using a knee support with a patellar guiding ring - a prospective and randomized study, Combined
Congress of the International Arthroscopy Association and the International Society of the Knee, Hong
Kong, May 1995.
120. Aglietti P, Buzzi R, Insall JN. Disorders of the patellofemoral joint. In: Insall JN, Windsor RE, Scott
WN, et al, eds. Surgery of the Knee, ed 2. New York: Churchill Livingstone, 1993; pgs 241-385.
121. Kolowich PA, Paulos LE, Rosenberg TD, et al. Lateral release of the patella: Indicatins and
contraindicaations, Am J Sports Med 1990; 18:359-365.
122. Kelly MA. Algorithm for anterior knee pain. In: Cannon WD Jr., ed. Instructional Course Lectures.
IL: AAOS, 1998;pgs 339-343.
123. Post WR, Fulkerson J. Knee Pain Diagrams: Correlation with Physical Examination Findings in
Patients with Anterior Knee Pain, Arthroscopy 1994;10(6)618-23.
124. Novacheck TF. Running injuries: a biomechanical approach. In: Cannon WD Jr., ed. Instructional
Course Lectures. IL: AAOS, 1998;pgs 397-406.
125. Mori Y, Kuroki Y, Yamamoto R, Fujimoto A, Okumo H, Kubo M. Clinical and histological study of
patellar chondropathy in adolescents. Arthroscopy 1991;7(2):182-97.
126. Hayes CW. MRI of the Patellofemoral Joint, Semin Ultrasound-CT-MR 1994;15(5):383-95.
127. Rose PM, Demlow TA, Szumowski J, Quinn SF. Chondromalacia Patellae: Fat-Suppressed MR
imaging, Radiology 1994;193(2):437-40.
128. Gagliardi JA, Chung EM, Chandnani VP, Kesling KL, Christensen KP, Null, RN, Radvany MG, Hansen
MF. Detection and Staging of Chondromalacia Patellae: Relative Efficacies of Conventional MR Imaging,
MR Arthrography and CT Arthrography, AJR Am J Roentgenol 1994;163(3):629-36.
129. Ettinger WH, Davis MA, Neuhaus JM, Mallon KP. Long-term physical functioning in persons with
knee osteoarthritis from NHANES. I: effects of comorbid medical conditions, J Clin Epidemiol
1994;47(7):809-15.
130. Maffulli N, Testa V, Capasso G. Mediopatellar synovial plica of the knee in athletes: results of
arthroscopic treatment. Med Sci Sports Exerc 1993;25(9):985-8.
131. Shea KP, Fulkerson JP. Preoperative computed tomography scanning and arthroscopy in predicting
outcome after lateral retinacular release. Arthroscopy 1992;8(3):327-34.
132. Abernethy PJ, Townsend PR, Rose RM, Radin EL. Is chondromalacia patellae a separate clinical
entity?. J Bone Joint Surg [Br] 1978;60-B(2):205-10.
133. Maquet P. Mechanics and osteoarthritis of the patellofemoral joint. Clin Orthop 1979;(144):70-3.
134. Villar RN. Patellofemoral pain and the infrapatellar brace. A military view. Am J Sports Med
198;13(5):313-5.
135. Post WR. History and physical examination. IN: Fulkerson JP, ed. Disorders of the Patellofemoral
Joint. London: Williams & Wilkins, 1997;39-71.
136. Dzioba RB. Diagnostic arthroscopy and longitudinal open lateral release. A four year follow-up
study to determine predictors of surgical outcome. Am J Sports Med 1990;18(4):343-8.
137. Jones RB, Barlett EC, Vainright JR, Carroll RG. CT Determination of tibial tubercle lateralization in
patients presenting with anterior knee pain, Skeletal Radiol 1995;24(7)505-9.
138. Poehling GG, Pollock FE Jr., Koman LA. Reflex sympathetic dystrophy of the knee after sensory
nerve injury, Arthrosocpy 1988;4:31-5.
139. Cooper DE, DeLee JC. Reflex sympathetic dystrophy of the knee, J Am Acad Orthop Surg
1994;2:79-86.
140. Cooper De, DeLee JC, Ramamurthy S. Reflex sympathetic dystrophy of the knee. Treatment using
continuous epidural anesthesia, J Bone Joint Surg 1989;71A:365-369.
141. Finsterbush A, Frankl U, Mann G, Lowe J. Reflex Sympathteic Dystrophy of the Patello-femoral
Joint. Orthop Rev. 1991;20:877-885.
142. Dzioba RB. Diagnostic arthroscopy and longitudinal open lateral release. A four year follow-up
study to determine predictors of surgical outcome. Am J Sports Med 1990;18(4):343-8.
143. Malhotra R, Dhingra SS, Padhy AK, Kumar R, Ravishankar U. Reflex sympathetic dystrophy of
patello-femmoral joint. Diagnosis and Relevance, Clin Nucl Med 1995;20(12):1058-60.
144. Voight ML, Wieder DL. Comparative reflex response times of vastus medialis obliquus and vastus
lateralis in normal subjects and ubjects with extensor mechanism dysfunction. An electromyographic
study. Am J Sports Med 1991;19(2):131-7.
145. Smith AD, Stroud L, McQueen C. Flexibility and anterior knee pain in adolescent elite figure
skaters. J Pediatr Orthop 1991;11(1):77-82.
146. Romanoff ME, Cory PC Jr, Kalenak A, Keyser GC, Marshall WK. Saphenous nerve entrapment at the
adductor canal. Am J Sports Med 1989;17(4):478-81.
147. Mori Y, Kubo M, Shimokoube J, Kuroki Y. Osteochondritis dissecans of the patellofemoral groove in
athletes: unusual cases of patellofemoral pain. Knee Surg Sports Traumatol Arthrosc 1994;2(4):242-4.
148. Fu FH, Maday MG. Arthroscopic lateral release and the lateral patellar compression syndrome.
Orthop Clin North Am 1992;23(4):601-12.
149. Vaatainen U, Hakkinen T, Kiviranta I, Jaroma H, Inkinen R, Tammi M. Proteoglycan Depletion and
size reduction in lesions of early grade chondromalacia of the patella, Ann Rheum Dis 1995;54(10):831-
5.
150. Vaatainen U, Airaksinen O, Jaroma H, Kiviranta I. Decreased torque and electromyographic activity
in the extensor thigh muscles in chondromalacia patellae, Int J Sports Med 1995;16(1):45-50.
151. Butler JP, Saddler S, Hill JA. An Intermeniscal fibrous band in a recreational runner, Arthroscopy
1995;11(6):735-7.
152. Campagnolo DI, Davis BA, Blacksin MF. Computed tomography-guided aspiration of a ganglion
cyst of the anterior cruciate ligament: a case report. Arch Phys Med Rehabil 1996;77(7):732-3.
153. Kang CN, Lee SB, Kin SW. Symptomatic ganglion cyst within the substance of the anterior cruciate
ligament. Arthroscopy 1995;11(5):612-5.
154. Watanabe BM, Howell SM. Arthroscopic findings associated with roof impingement of an anterior
cruciate ligament graft. Am J Sports Med 1995;23(5):616-25.
155. Tria AJ JR, Alicea JF, Cody RP. Patella baja in anterior cruciate ligament reconstruction of the knee.
Clin Ortho 1994;299:229-34.
156. Kleipool AE, Van-Loon T, Marti RK. Pain after use of the central third of the patellar tendon for
cruciate ligament reconstruction. 33 patients followed 2-3 years. Acta Ortho Scand 1994;65(1)62-6.
157. Shino K, Nakagawa S, Inoue M, Horibe S, Yoneda M. Deterioration of patellofemoral articular
surfaces after anterior cruciate ligament reconstruction. Am J Sports Med 1993;21(2):206-11.
158. Rosenberg TD, Franklin JL, Baldwin GN, Nelson KA. Extensor mechanism function after patellar
tendon graft harvest for anterior cruciate ligament reconstruction. Am J Sports Med 1992;20(5):519-
25; discussion 525-6.
159. Kartus J, Magnusson L, Stener S, Brandsson S, Eriksson BI, Karlsson J. Complications following
arthroscopic anterior cruciate ligament reconstruction. A 2-5 year follow-up of 604 patients with special
emphasis on anterior knee pain. Knee Surg Sports Traumatol Arthrosc 1999;7(1):2-8.,
160. Jarvela T, Kannus P, Jarvinen M. Anterior knee pain 7 years after an anterior cruciate ligament
reconstruction with a bone-patellar tendon-bone autograft. Scnad J Med Sci Sports 2000;10(4):221-
227.
161. Banky, et al. J Noc Med 1994;35:855-62.
162. Homminga GN, Mazee HA, Van der Linden ES, Van Ooy A. Delayed intraosseous venous blood flow
does not correlate with patellar cartilage changes in anterior knee pain. Acta Orthop Belg
1995;61(2):79-82.
163. Magi M, Branca A, Bucca C, Langerame V. Hoffa disease. Ital J Orthop Traumatol 1991;17(2):211-
6.
164. Krebs VE, Parker RD. Arthroscopic resection of an extrasynovial ossifying chondroma of the
infrapatellar fat pad: end-stage hoffa's disease?. Arthroscopy 94;10(3):301-4.
165. Methaeny J, Mayor M. Am J Knee Surg 1988;1:134-9.
166. Ogata K. Painful bipartite patella. A new approach to operative treatment. J Bone Joint Surg
1994;76A(4):573-8.
167. Ireland ML, Chang JL. Acute fracture bipartite patella: case report and literature review. Med & Sci
Sports and Exercise 1995;299-302.
168. Eckhoff DG, Montgomery WK, Kilcoyne RF, Stamm ER. Femoral morphometry and anterior knee
pain, Clin Orthop 1994;302:64-8.
169. Reider B, Marshall JL, Warren RF. Clinical characteristics of patellar disorders in young athletes.
Am J Sports Med 1981;9(4):270-4
170. Pinar H, Akseki D, Karaoglan O, Genc I. Kinematic and dynamic axial computed tomography of the
patello-femoral joint in patients with anterior knee pain. Knee Surg Sports Traumatol Arthrosc
1994;2(3):170-3.
171. Meister K, James SL. Proximal tibial derotation osteotomy for anterior knee pain in the miserably
malaligned extremity. Am J Orthop 1995;24(2):149-55.
172. Fulkerson JP, Shea KP. Disorders of patellofemoral alignment. J Bone Joint Surg [Am]
1990;72(9):1424-9.
173. An KN, Chao EYS, Kaufman KR. Analysis of muscle and joint loads. IN: Mow VC, Hayes WC, eds.
Basic Orthopaedic Biomechanics. New York: Raven Press, 1991;1-50.
174. Mori Y, Fujimoto A, Okumo H, Kuroki Y. Lateral retinaculum release in adolescent patellofemoral
disorders: its relationship to peripheral nerve injury in the lateral retinaculum. Bull Hosp Jt Dis Orthop
Inst 1991 Fall;51(2):218-29.
175. Wojtys EM, Beaman DN, Glover RA, Janda D. Innervation of the human knee joint by substance-P
fibers. Arthroscopy 1990;6(4):254-63.
176. Caylor D, Fites R, Worrell TW. The relationship between quadriceps angle and anterior knee pain
syndrome. J Orthop Sports Phys Ther 1993;17(1):11-6.
177. Quaile A. Measurement of the effects of lateral release. J R Nav Med Serv 1989 Winter;75(3):159-
63.
178. Koskinen SK, Hurme M, Kujala UM, Kormano Ml. Effect of lateral release on patellar motion in
chondromalacia. An MRI study of 11 knees. Acta Orthop Scand 1990;61(4):311-12.
179. Lossifidis A, Brueton RN. Painful bipartite patella following injury. Injury 1995;26(3):175-6.
180. Novacheck TF. Walking, running and sprinting: a three-dimensional analysis of kinematics and
kinetics. IN: Jackson DW, ed. Instructional Course Lectures 44. IL: AAOS, 1995;497-506.
181. Seedhom BB. Mechanical Factors and Osteoarthrosis I: Hypothesis, Proceedings Israel Society of
Sports Medicine, Tel Aviv, Israel 1992;24-25.
182. Seedhom BB, Swann AC. Mechanical Factors and Osteoarthrosis II: Does Cartilage Stiffness Adapt
to the Prevalent Stress?, Proceedings Israel Society of Sports Medicine, Tel Aviv, Israel 1992;26.
183. Hungerford DS, Barry M. Biomechanics of the patellofemoral joint, Clin Orthop 1979;144:11.
184.Buckwalter JA, Martin J. Degenerative joint disease. Clinical Symposia 1995;47(2).
185. Panush RS, Schmidt C, Caldwell JR, et al. Is running associated with degenerative joint disease?. J
Am Med Assoc 1986;255(9):1152-4.
186. Lane NE, Bloch DA, Wood PD, Fries JF. Aging, long-distance running, and the development of
musculoskeletal disability. A controlled study. Am J Med 1987; 82(4):772-80.
187. Panush RS. Does exercise cause arthritis? Long-term consequences of exercise on the
musculoskeletal system. Rheumat Dis Clin. North Am 1990;16(4):827-36.
188. Lane NE, Bloch DA, Hubert HB, et al. Running, osteoarthritis, and bone density: initial 2-year
longitudinal study. Am J Med 1990;88(5):452-9.
189. Lane NE, Michel B, Bjorkengren A, et al. The risk of osteoarthritis with running and aging: a 5-year
longitudinal study. J Rheumatol 1993;20(3):461-8.
190. Lane NE, Bloch DA, Jones HH, et al. Long-distance running, bone density, and osteoarthritis. J Am
Med Assoc 1986;255(9):1147-51.
191. Tammi M, Paukkonen K, Kiviranta I, Jurvelin J, et al. Joint loading-induced alterations in articular
cartilage. IN: Helminen HJ, Kiviranta I, Tammi M, Säämänen AM, et al, eds. Joint loading: biology and
health of articular structures. England: John Wright (Butterworths), 1987;64-88.
192. Helminen HJ, Kiviranta I, Säämänen AM, Jurvelin JS, et al. Effect of motion and load on articular
cartilage in animal models. IN: Kuettner KE, Schleyerbach R, Peyron JG, Hascall VC, eds. Articular
Cartilage and Osteoarthritis. New York: Raven Press 1992;501-10.
193. Dye SF, Vaupel GL, Dye CC, Allen GW, et al. Conscious neurosensory mapping of the internal
structures of the human knee without intra-articular anesthesia, Proceedings of 1st Biennial ISAKOS
Congress, Buenos Aires, Argentina, May 1997.
194. Fife RS, Brandt KD, Braunstein EM, et al. Musculoskeletal System. Relationship between
arthroscopic evidence of cartilage damage and radiographic evidence of joint space narrowing in early
osteoarthritis of the knee. Arthritis Rheum 1991;34:337-82.
195. Walker C, Cassar-Pullicino VN, Vaisha R, McCall IW. The patello-femoral joint--a critical appraisal
of its geometric assessment utilizing conventional axial radiography and computed arthro-tomography.
Br J Radiol 1993;66(789):755-61.
196. Quinn SF, Rose PM, Brown TR, Demlow TA. MR Imaging of the patellofemoral compartment. MRI
Clin N AM 1994;2(3):425-40.
197. Andresen R, Radmer S, Konig H, Banzer D, Wolf KJ. MR diagnosis of retropatellar condral lesions
under compression. A comparison with histological findings. Acta Radiol 1996;37(1):91-7.
198. Hodge JC, Ghelman B, O'Brien SJ, Wickiewicz TL. Synovial plicae and chondromalacia patellae:
correlation of results of CT arthrography with results of arthroscopy. Radiology 1993;186(3):827-31.
199. Hansen H, Boe S. The pathological plica in the knee. Results after arthroscopic resection. Arch
Orthop Trauma Surg 1989;108(5):282-4.
200. Hansen H, Boe S. The pathological Plica in the knee. Results after arthroscopic resection. Arch
Ortho Tr Surg 1989;108:282-4.
201. Harilainen A, Sandelin J. Prospective Long-Term Results of Operative Treatment in Primary
Dislocation of the Patella, Knee Surg Sports Traumatol Arthroscopy 1993;1(2):100-3.
202. Kin HKW, Salter RB. The potential for regeneration of articular cartilage in defects created by
chondral shaving and subchondral abrasion, J Bone Joint Surg 1991;73A:1301-?.
203. McConnell J. The management of chondromalacia patellae: a long term solution, Aust J
Physiotherapy 1986;32:215-223.
204. Yates C, Grana WA. Patellofemoral pain--a prospective study. Orthop 1986;9(5):663-7.
205. Wilson KC, Evans-Smith E, Oelman BJ. A study of patellofemoral plain in a junior infantry training
unit. J R Army Med Corps 1983;129(2):82-7.
206. Almekinders LC, Almekinders SV. Outcome in the treatment of chronic overuse sports injuries: a
retrospective study. J Ortho Sports Phys Ther 1994;19(3):157-61.
207. Casscells SW. Chondromalacia of the patella. J Pediatr Orthop 1982;2(5):560-4.
208. Whitelaw GP Jr, Rullo DJ, Markowitz HD, Marandola MS, DeWaele MJ. A conservative approach to
anterior knee pain. Clin Orthop 1989;(246):234-7.
209. Ruffin MT 5th, Kiningham RB. Anterior knee pain: the challenge of patellofemoral syndrome. Am
Fam Physician 1993;47(1):185-94.
210. Jensen DB, Albrektsen SB. The natural history of chondromalacia patellae. A 12-year follow-up.
Acta Orthop Belg 1990;56(2):503-6.
211. Edeen J, Dainer RD, Barrack RL, Alexander AH. Results of conservative treatment for recalcitrant
anterior knee pain in active young adults. Orthop Rev 1992;21(5):593-9.
212. Quaile A. Measurement of the effects of lateral release. J R Nav Med Serv 1989 Winter;75(3):159-
63.
213. Almekinders LC, Almekinders SV. Outcome in the treatment of chronic overuse sports injuries: a
retrospective study. J Orthop Sports Phys Ther 1994;19(3):157-61.
214. Post WR, Fulkerson JP. Anterior knee pain--a symptom not a diagnosis. Bull Rheum Dis
1993;42(2):5-7.
215. Weaver JK, Wieder D, Derkash RS. Patellofemoral arthritis resulting from malalignment. A
long-term evaluation of treatment options. Orthop Review 1991;20:1075-81.
216. Vaquero J, Arriaza R. The patella thinning osteotomy. An experimental study of a new technique
for reducing patellofemoral pressure. Int Orthop 1992;16(4):372-6.
217. Lennox IA, Cobb AG, Knowles J, Bentley G. Knee function after patellectomy. A 12 to 48 year
follow-up. Br J Bone Joint Surg 1994;76(3):485-7.
218. Manicol MF. Patellar Osteotomy for intractable patellar pain. Indian Artho Society Newsletter
1997;12.
219. Lowe J, Mann G, Matan Y, Finsterbush A, Frankl U, et al. Shoe and insole effect on medical
complaints, overuse injuries and stress fractures in infantry recruits - a prospective, randomized study-
preliminary results. Proceedings of the Congress of the International Arthroscopy Association and the
International Society of the Knee, Hong Kong, May 1995.
220. Woodland LH, Francis RS. Parameters and comparisons of the quadriceps angle of college-aged
men and women in the supine and standing positions. Am J Sports Med 1992;20(2):208.
221. Fulkerson JP. Biomechanics of the patellofemoral joint. IN: Fulkerson JP, ed. Disorders of the
Patellofemoral Joint. London: Williams & Wilkins, 1997;23-38.
222. Fulkerson JP. Reflex sympathetic dystrophy and chronic pain. IN: Fulkerson JP, ed. Disorders of
the Patellofemoral Joint. London: Williams & Wilkins, 1997;337-51.
223. Katz M, Hungerford DS. Reflex sympathetic dystrophy affecting the knee. J Bone Joint Surg
1987;69B:797-803.
224. Butler-Manuel PA, Justins D, Heatley FW. Sympathetically mediated anterior knee pain.
Scintigraphy and anesthetic blockade in 19 patients. Acta Orthop Scand 1992;63(1):90-93.
225. Ben-Eliyahu DJ. Infrared thermographic imaging in the detection of sympathetic dysfunction in
patients with patellofemoral pain syndrome (published erraturm appears in J Manipulative Physiol Ther
1992;15(6) - preceding table of contents) J Manipulative Physiol Ther 1992;15(3):161-70.
226. Fulkerson JP, Hungerford DS, Ficat RP. Disorders of the Patellofemoral Joint, ed 2. Maryland:
Williams & Wilkins, 1990.
227. Hoppenfeld Stanley. Physical examination of the spine and extremities. New York: Appleton-
Centruy-Crofts, 1976.
228. Laurin CA, Dussault R, Levesque HP. The tangential x-ray investigation of the patellofemoral joint:
x-ray technique, diagnostic criteria and their interpretation. Clin Orthop 1979;144(Oct):16-26.
229. Radin EL. A rational approach to the treatment of patello-femoral pain. Clin Orthop 1979;144:107-
109.
230. Fulkerson JP. Disorders of the patello-femoral joint. Lippincott Williams & Wilkins, 2004, p. 143-
145.
231. Grana WA & Kriegshauser LA. Scientific basis of extensor mechanism disorders. Clin Sports Med
1985;4:247-257.
232. Agglieti P, Buzzi R, Insall J. Disorders of the Patello-femoral joint in: Surgery of the Knee, ed.
Insall & Scott, Churchill-Livingstone, 2001. p. 922-923.
233. Post WR. Anterior Knee Pain: Diagnosis and Treatment. J Am Acad Orthop Surg 2005;13:534-
543.
234. Biedert RM, Stauffer E, Friederich NF. Occurrence of free nerve endings in the soft tissue of the
knee joint. An histologic investigation. Am J Sports Med 1992;20(4):430-433.
235. Dye SF, Vaupel GL, Dye CC. Conscious neurosensory mapping of the internal structures of the
human knee without intraarticular anesthesia. Am J Sports Med 1998;26:773-777
236. Sanchis-Alfonso V, Rosello-Sastre E, Monteagudo-Castro C, Esquerdo J. Quantitative analysis of
nerve changes in the lateral retinaculum in patients with isolated symptomatic patellofemoral
malalignment. A preliminary study. Am J Sports Med 1998;26(5):703-709.
237. Sanchis-Alfonso V, Rosello-Sastre E, Revert F. Neural growth factor expression in the lateral
retinaculum in painful patellofemoral malalignment. Acta Orthop Scand 2001;72:146-149.
238. Sanchis-Alfonso V, Rosello-Sastre E. Immunohistochemical analysis for neural markers of the
lateral retinaculum in patients with isolated symptomatic patello-femoral malalignment. A
neruoanatomic basis for anterior knee pain in the active young patient. Am J Sports Med
2000;28(5):725-731.
239. Witonski D, Wagrowska-Danielewicz M. Distribution of substance-P nerve fibers in the knee joint in
patients with anterior knee pain syndrome. A preliminary report. Knee Surg Sports Traumatol Arhtrosc
1999;7(3):177-183.
240. Micheli LJ. Patellofemoral Disorders in Children. In: The Patellofemoral Joint. Fox JM & Del-Pizzo W
(eds.). McGraw-Hill Inc., N.Y. 1993; p. 105-121.
241. Kasim N, Fulkerson JP. Resection of clinically localized segments of painful retinaculum in the
treatment of selected patients with anterior knee pain. Am J Sports Med 2000;28(6):811-814.
242. Cowan SM, Bennell KL, Hodges PW, Crossley KM, McConnell J. Delayed onset of electromyographic
activity of vastus medialis obliquus relative to vastus lateralis in subjects with patellofemoral pain
syndrome. Arch Phys Med Rehabil 2001;82:183-189.
243. Owings TM, Grabiner MD. Motor control of the vastus medialis oblique and vastus lateralis muscles
is disrupted during eccentric contractions in subjects with patellofemoral pain. Am J Sports Med
2002;30:483-487.
244. Cesarelli M, Bifulco P, Bracale M. Quadriceps muscles activation in anterior knee pain during
isokinetic exercise. Med Eng Phys 1999;21(6-7):469-478.
245. Witvrouw E, Lysens R, Bellemans J, Cambier D, Vanderstraeten G. Intrinsic risk factors for the
development of anterior knee pain in an athletic population. A two-year prospective study. Am J Sports
Med 2000;28(4):480-489.
246. Duffey MJ, Martin DF, Cannon DW, Craven T, Messier SP. Etiologic factors associated with anterior
knee pain in distance runners. Med Sci Sports Exerc 2000;32(11):1825-1832.
247. Popp JE, Yu JS, Kaeding CC. Recalcitrant patellar tendinitis: Magnetic resonance imaging, histologic
evaluation, and surgical treatment. Am J Sports Med 1997;25:218-222.
248. Voto SJ, Ewing JW. Retrotendinous calcification of the infrapatellar tendon: unusual cause of
anterior knee pain syndrome. Arthroscopy 1988;4(2):81-84.
249. Siebert CH, Kaufmann A, Niedhart C, Heller KD. The quadriceps tendon cyst: an uncommon cuase
of chronic anterior knee pain. Knee Surg Sports Traumatol Arthrosc 1999;7(6):349-351.
250. Pathak G, Atkinson RN. Patellar 'entry' feature: a new arthroscopic anatomic finding. Knee 2004
(Apr);11(2):99-101.
251. Meidan O. Activity related localized anterior knee pain on adolescence – A report of two uncommon
etiologies and differential diagnosis. In preparation, October 2006.
252. Eckstein F, Putz R, Muller-Gerbl M, Steinlechner M, Benedetto KP. Cartilage degeneration in the
human patellae and its relationship to the mineralisation of the underlying bone: a key to the
understanding of chondromalacia patellae and femoropatellar arthrosis? Surg Radiol Anat
1993;15(4):279-286.
253. Goodfellow J, Hungerford DS, Woods C. Patello-femoral joint mechanics and pathology. 2.
Chondromalacia patellae. J Bone Joint Surg Br 1976;58(3):291-299.
254. Outerbridge RE, Dunlop JA. The problem of chondromalacia patellae. Clin Orthop Relat Res 1975
(Jul-Aug);(110):177-196.
255. Joensen AM, Hahn T, Gelineck J, Overvad K, Ingemann-Hansen T. Articular cartilage lesions and
anterior knee pain. Scand J Med Sci Sports 2001 (Apr);11(2):115-119.
256. Price AJ, Jones J, Allum R. Chronic traumatic anterior knee pain. Injury 2000 (Jun);31(5):373-378.
257. Dye SF, Boll DA. Radionuclide imaging of the patellofemoral joint in young adults with anterior
knee pain. Orthop Clin North Am 1986;17:249-262.
258. Lee SH, Suh JS, Cho J, Kim SJ, Kim SJ. Evaluation of chondromalacia of the patella with axial
inversion recovery-fast spin-echo imaging. J Magn Reson Imaging 2001;13(3):412-416.
259. Macarini L, Perrone A, Murrone M, Marini S, Stefanelli M. Evaluation of patellar chondromalacia
with MR: comparison between T2-weighted FSE SPIR and GE MTC. Radiol Med (Torino)
2004;108(3):159-171.
260. Pookarnjanamorakot C, Jaovisidha S, Apiyasawat P. The patellar tilt angle: correlation of MRI
evaluation with anterior knee pain. J Med Assoc Thai 1998;81(12):958-963.
261. Metin-Cubuk S, Sindel M, Karaali K, Arslan AG, Akyildiz F, Ozkan O. Tibial tubercle position and
patellar height as indicators of malalignment in women with anterior knee pain. Clin Anat
2000;13(3):199-203.
262. Post WR, Teitge R, Amis A. Patellofemoral malalignment: Looking beyond the viewbox. Clin Sports
Med 2002;21:521-546.
263. Livingston LA, Mandigo JL. Bilateral Q angle asymmetry and anterior knee pain syndrome. Clin
Biomech (Bristol, Avon) 1999;14(1):7-13.
264. Witonski D, Goraj B. Patellar motion analyzed by kinematic and dynamic axial magnetic resonance
imaging in patients with anterior knee pain syndrome. Arch Orthop Trauma Surg 1999;119(1-2):46-49.
265. Sanchis-Alfonso V, Rosello-Sastre E, Martinez-Sanjuan V. Pathogenesis of anterior knee pain
syndrome and functional patello-femoral instability in the active young. Am J Knee Surg 1999
(Winter);12(1):29-40.
266. Fulkerson JP, Arendt EA. The female knee - anterior knee pain. Conn Med 1999;63(11):661-664.
267. Fulkerson JP, Arendt EA. Anterior knee pain in females. Clin Orthop 2000 (Mar);(372):69-73.
268. Laprade J, Culham E. Radiographic measures in subjects who are asymptomatic and subjects with
patellofemoral pain syndrome. Clin Orthop 2003;414:172-182.
270. Miltner O, Siebert CH, Schneider U, Niethard FU, Graf J. Patellar hypertension syndrome in
adolescence: A three-year follow up. Arch Orthop Trauma Surg 2003;123:455-459.
271. Schneider U, Breusch SJ, Thomsen M, Wenz W, Graf J, Niethard FU. A new concept in the
treatment of anterior knee pain: patellar hypertension syndrome. Orthopedics 2000;23(6):581-586.
272. Hetsroni I, Finestone A, Milgrom C, Ben Sira D, Nyska M, Radeva-Petrova D, Ayalon M. A
prospective biomechanical study of the association between foot Pronation and the incidence of anterior
knee pain among military recruits. J Bone Joint Surg Br 2006;88-B:905-908.
273. Post WR, Fulkerson J. Knee pain diagrams: Correlation with physical examination findings in
patients with anterior knee pain. Arthroscopy 1994;10:618-623.
274. Thomee P, Thomee R, Karlsson J. Patellofemoral pain syndrome: pain coping strategies and degree
well-being. Scand J Med Sci Sports 2002;12(5):276-781.
275. Witonski D. Anterior knee pain syndrome. Int Orthop 1999;23(6):341-344.
276. Andrish J. Personal communication, April 26, 2006.
277. Willson JD, Dougherty CP, Ireland ML, McClay Davis I. Core Stability and its relationship to lower
extremity function and injury. J Am Acad Orthop Surg 2005;13:316-325.
278. Suter E, McMorland G, Herzog W, Bray R. Decrease in quadriceps inhibition after sacroiliac joint
manipulation in patients with anterior knee pain. J Manipulative Physiol Ther 1999;22(3):149-153.
279. Baker V, Bennell K, Stillman B, Cowan S, Crossley K. Abnormal knee joint position sense in
individuals with patellofemoral pain syndrome. J Orthop Res 2002;20:208-214.
280. Ireland ML, Willson JD, Ballantyne BT, Davis IM. Hip strength in females with and without
patellofemoral pain. J Orthop Sports Phys Ther 2003;33:671-676.
281. Zhang SN, Bates BT, Dufek JS. Contributions of lower extremity joints to energy dissipation during
landings. Med Sci Sports Exerc 2000;32:812-819.
282. Van-Tiggelen D, Witvrouw E, Roget P, Cambier D, Danneels L, Verdonk R. Effect of bracing on the
prevention of anterior knee pain – a prospective randomized study. Knee Surg Sports Traumatol
Arthrosc 2004 (Sep);12(5):434-439.
283. Doucette SA, Goble EM. The effect of exercise on patellar tracking in lateral patellar compression
syndrome. Am J Sports Med 1992;20:434-440.
284. Kannus P, Natri A, Paakkala T, Jarvinen M. An outcome study of chronic patellofemoral pain
sydrome: Seven-year follow-up of patients in a randomized, controlled trial. J Bone Joint Surg Am
1999;81:355-363.
285. Bennett JG, Stauber WT. Evaluation and treatment of anterior knee pain using eccentric exercise.
Med Sci Sports Exerc 1986;18(5):526-530.
286. Lam PL, Ng GY. Activation of the quadriceps muscle during semisquatting with different hip and
knee positions in patients with anterior knee pain. Am J Phys Med Rehabil 2001;80(11):804-808.
287. Herbert R. Exercise, not taping, improves outcomes for patients with anterior knee pain. Aust J
Physiother 2001;47(1):66.
288. Powers CM, Landel R, Sosnick T, et al. The effects of patellar taping on stride characteristics and
joint motion in subjects with patellofemoral pain. J Orthop Sports Phys Ther 1997;26:286-291.
289. Cowan SM, Bennell KL, Hodges PW. Therapeutic patellar taping changes the timing of vasti muscle
activation in people with patellofemoral pain syndrome. Clin J Sport Med 2002;12:339-347.
290. Roush MB, Sevier TL, Wilson JK, Jenkinson DM, Helfst RH, Gehlsen GM, Basey AL. Anterior knee
pain: a clinical comparison of rehabilitation methods. Clin J Sport Med 2000;10(1):22-28.
291. Clark DI, Downing N, Mitchell J, Coulson L, Syzpryt EP, Doherty M. Physiotherapy for anterior knee
pain: a randomized controlled trial. Ann Rheum Dis 2000;59(9):700-704.
292. Powers CM, Shellock FG, Beering TV, Garrido DE, Goldbach RM, Molnar T. Effect of bracing on
patellar kinematics in patients with patello-femoral joint pain. Med Sci Sports Exerc 1999;31(12):1714-
1720.
293. Hartig DE, Henderson JM. Increasing hamstring flexibility decreases lower extremity overuse
injuries in military basic trainees. Am J Sports Med 1999;27(2):173-176.
294. Crossley K, Bennell K, Green S, Cowan S, McConnell J. Physical therapy for patellofemoral pain: A
randomized, double-blinded, placebo-controlled trial. Am J Sports Med 2002;30:857-865.
295. Federico DJ, Reider B. Results of isolated patellar debridement for patellofemoral pain in patients
with normal patellar alignment. Am J Sports Med 1997;25:663-669.
296. Owens BD, Stickles BJ, Balikian P, Busconi BD. Prospective analysis of radiofrequency versus
mechanical debridement of isolated patellar chondral lesions. Arthroscopy 2002;18:151-155.
297. Ryan A, Bertone AL, Kaeding CC, Backstrom KC, Weisbrode SE. The effects of radiofrequency
energy treatment on chondrocytes and matrix of fibrillated articular cartilage. Am J Sports Med
2003;31:386-391.
298. Mann G. Anterior Knee Pain Syndrome. In: Sports Injuries, Arthroscopy and Joint Surgery. Current
Trends and Concepts. Doral MN, Leblebicioglu G, Atay OA, Baydar ML (eds). Ankara 2000, p.115-129.
299. Brittberg M, Lindahl A, Nilsson A, Ohlsson C, Isaksson O, Peterson L. Treatment of deep cartilage
defects in the knee with autologous chondrocyte transplantation. N Engl J Med 1994;331:889-895.
300. Peterson L, Minas T, Brittberg M, Nilsson A, Sjogren-Jansson E, Lindahl A. Two-to 9-year outcome
after autologous chondrocyte transplantation of the knee. Clin Orthop 2000;374:212-234.
301. Minas T. Autologous chondrocyte implantation for focal chondral defects of the knee. Clin Orthop
2001;391:S349-S361.
302. Peterson L, Brittberg M, Kiviranta I, Akerlund EL, Lindahl A. Autologous chondrocyte
transplantation: Biomechanics and long-term durability. Am J Sports Med 2002;30:2-12.
303. Bartlett W, Gooding CR, Carrington RW, Skinner JA, Briggs TW, Bentley G. Autologous chondrocyte
implantation at the knee using a bilayer collagen membrane with bone graft. A preliminary report. J
Bone Joint Surg Br 2005;87(3):330-332.
304. Knutsen G, Engebretsen L, Ludvigsen TC, et al. Autologous chondrocyte implantation compared
with micro-fracture in the knee: A randomized trial. J Bone Joint Surg Am 2004;86:455-464.
305. Shea KP, Fulkerson JP. Preoperative computed tomography scanning and arthroscopy in predicting
outcome after lateral retinacular release. Arthroscopy 1992;8:327-334.
306. Fulkerson JP. Diagnosis and treatment of patients with patellofemoral pain. Am J Sports Med
2002;30:447-456.
307. Dye SF. The knee as a biologic transmission with an envelope of function: A theory. Clin Orthop
1996;325:10-18.
308. Harper WM, Wray CC, Burden AC. An unusual cause of flexion deformity of the hips and knees. A
case report. Bone Joint Surg [Am] 1989 Oct;71(9):1418.
309. Fredericson M. Common injuries in runners; diagnosis, rehabilitation and prevention. Sports Med
1996;21:49-72.
310. Powell KE, Kohl HW, Caspersen CJ, Blair SN. An epidemiological perspective on the cause of
running injuries. Physician Sports Med 1986;14:100-114.
311. Jacobs SJ, Berson BL. Injuries to runners: a study of entrants to a 10,000 meter race. Am J sports
Med 1986;14:151-155.


Platelet rich plasma: any substance into it?

Omer Mei-Dan 1, Gideon Mann 1, 2


, Nicola Maffulli 3

1. Department of Orthopaedic Surgery, Sports Injury Unit, Meir University Hospital,


Kfar-Saba, Israel
2. Ribstein Center for Sport Medicine Sciences and Research, Wingate Institute,
Netanya, Israel
3. Queen Mary University of London, Centre for Sports and Exercise Medicine,
Barts and The London School of Medicine and Dentistry Mile End Hospital, 275
Bancroft Road London E1 4DG England

Tel: + 44 20 8223 8839


Fax: + 44 20 8223 8930
n.maffulli@qmul.ac.uk

*** This paper has been printed with permission of British Journal of
Sports Medicine

Keywords: PRP, platelet-rich plasma, sports medicine

Autologous platelet-rich plasma (PRP) is perceived to accelerate healing in


musculoskeletal injuries. PRP is increasingly used in situations that require rapid
return-to-play, which, in the professional sports arena, translates to fame and
money. It is astonishing but understandable that the most influential stimulus for
PRP therapy in the US, years after the method had been popularized in Europe,
was a February 2009 article in the lay press (New York Times, Alan Schwarz,
http://www.nytimes.com/2009/02/17/sports/17blood.html?_r=1&scp=2&sq=prp&
st=cse).
Biological background:

Human blood platelet counts are approximately 200,000/mL. PRP is an


autologous concentration of human platelets above this in a small volume of
plasma 1. Reports vary regarding the platelet concentration and different growth
factors (GF) present in the PRP concentrate. Also, there are many preparation
protocols, kits, centrifuges, and methods to trigger platelet activation before use.
The same is true for application methods, including using injectable activated PRP
liquid concentrate versus implanting a fibrin scaffold, optimal timing of injection,
and the specific volume to use. Almost every major manufacturer in the orthopedic
and sports medicine world markets a different commercial kit. Some claim to
produce a better quantity and quality of PRP than their competitors from the same
amount of blood from the same patient. Costs vary tremendously: a commercial kit
yields a PRP concentrate at the cost of several hundred dollars, but in house non-
automatised techniques produce a PRP concentrate for around 10 dollars. Each
method to concentrate platelets leads to a different product with different biology
and potential uses 2, with a high variation (3- to 27-fold) in GF concentration and
2, 3, 4
in the kinetics of release . Most techniques yield a PRP concentrate of around
10% of the blood volume taken (e.g 20 mL of whole blood would result in
approximately 2 mL of PRP). These differences might be of relevance to clinical
2
management , although they have not been systematically studied. PRP
preparations containing only moderately elevated platelet concentrations may be
the ones to induce optimal biological benefit, with lower platelet concentrations
5, 6
leading to suboptimal effects, and higher ones to inhibitory effects . Other
authors have stated that the ‘therapeutic dose’ of PRP would be at least 4-6 times
7, 8
higher than the normal platelet count . To complicate things, the actual GF
content is not well correlated with the platelet count in whole blood or in PRP, and
there is no evidence that gender or age affects platelet count or GF concentrations
9
.

A few studies have categorized the different platelet concentrates according to


the presence or absence of white blood cells (WBC): either pure platelet-rich
plasma (P-PRP), in which WBC have been intentionally eliminated from the PRP, or
leukocyte and platelet-rich plasma (L-PRP) 2, possibly from the inability of the kit
to differentiate between the WBC and the PRP layers. A positive or negative effect
of WBC cannot be generalized to all tissues and clinical conditions. This issue
requires further investigation, as the WBC content in the preparation injected has
never been systematically studied. We do know that neutrophils promote additional
muscle damage soon after the initial injury, but there is no direct evidence that
3, 10
neutrophils play a beneficial role in muscle repair or regeneration . This
exacerbation of injury and/or delay in muscle regeneration may be of major
importance for injuries managed with PRP. This, together with the improved
homogeneity of P-PRP and its reduced donor-to-donor variability, supports some
3, 5
PRP production techniques that claim to be clinically superior . L-PRP injected for
soft tissue injuries might induce more local pain than P-PRP. Platelets by
11
themselves do reduce pain . L-PRP reduces post-operative pain, although here
12
the contribution of the WBC to the overall effect observed remains unclear .

Clinical rationale:

Platelets contain many biologically active factors, including many of the proteins
responsible for haemostasis, synthesis of new connective tissue, and
revascularization. They can stimulate a supra-physiologic release of GF to
jumpstart healing in chronic injuries, or speed up an acute injury repair process.
The idea behind PRP treatment is that all stages of the repair process are
controlled by a wide variety of cytokines and growth factors acting locally as
regulators of the most basic cell functions, using endocrine, paracrine, autocrine
and intracrine mechanisms 5. More than 95% of pre-synthesized GF are secreted
within one hour of activation from the alpha granules. After the initial burst of PRP-
related GF, platelets synthesize and secrete additional GF for the remaining seven-
8, 13
to-ten days of their life span . Typically, blood, such as the haematoma formed
in a muscle tear, contains about 94% red blood cells (RBC), a small amount of
platelets (6%), and less than 1% leukocytes. The rationale for PRP therapy lies in
reversing the blood ratio by decreasing RBC, which are less useful in the healing
process, to around 5%, and increasing platelet amount to 94% to stimulate
3, 8
recovery .
The main GF in the PRP concentrate are the transforming growth factor-ß1 (TGF-
ß1), platelet-derived growth factor (PDGF), vascular endothelial growth factor
(VEGF), epithelial growth factor (EGF), hepatocyte growth factor (HGF), and
insulin-like growth factor (IGF-I). Most of these GF play key roles in tendon,
muscle, ligament, cartilage and bone healing by stimulating angiogenesis,
epithelialization, cell differentiation- replication-proliferation, and formation of
14, 15, 16
extracellular matrix .

Most early studies concentrated on purified isolated GF which were known to


have a specific role in tissue healing. Only in the past decade has it been
recognized and put into practice that the need to target various signaling pathways
requires the administration of a balanced combination of mediators, as isolated GF
would not be able to satisfy the multiple requirements of the injured tissue. PRP
17 18,
has been used to enhance the healing of meniscus defects and muscle injuries
19 16
, and stimulate chondrocytes to engineer cartilaginous tissue , reduce pain and
20
produce better and more balanced synovial fluid in arthritic knees , improve
21 18
outcomes after total knee arthroplasty and subacromial decompression ,
22
accelerate bone formation , stimulate the healing of an ACL central defect, its
23, 24
primary repair or its reconstruction , improve the outcome of operated
14 25
ruptured Achilles tendons , reduce pain in chronic tendinopathies , and prevent
26
and reverse intervertebral disc degeneration . However, the efficacy of PRP in
13
spinal fusion has been questioned . It is remarkable that very few randomized
controlled trials have been performed, and even less trials are adequately
powered, use appropriate outcome measures, and have decent follow up.

The 2008 “Aspetar Consensus”, organized by the World Anti-doping Association


(WADA) and the International Olympic Committee (IOC) to debate possible
27
conflicts with the WADA code, discussed the use of PRP in muscle injuries ,
concluding that further research is necessary. “The application of the WADA
Therapeutic Use Exemption (TUE) process is the preferred approach when wishing
to utilize GF technology in elite athletes, however the ability of the TUE committee
to appropriately evaluate such applications is inhibited by the current level of
scientific evidence”. The position statement concludes that “WADA will not be in a
position to evaluate its clinical utility for either assessment of TUE applications or
the prohibited list”. In section S2 of the Aspetar Consensus, concerning any
autologous product that contains GF, the only actual factor mentioned in
connection with PRP is IGF-1 which, while present in PRP, is systemically
subtherapeutic by a factor of 500: only 1% of it is unbound, available and active,
with a half life of 10 minutes (3,28).

Another concern is that PRP might produce genetic instability, potentially leading
to neoplasms. GFs act on cell membranes rather than on the cell nucleus, and
activate gene expression via internal cytoplasmic signal proteins, which promote
normal, not abnormal, gene expression 1. GF are not directly mutagenic, and act
through gene regulation and normal wound healing feedback control mechanisms.
Furthermore, the systemic effects on circulating GF from a local PRP injection
29
showed a very brief reduction of blood GF .

The modalities of use of PRP vary. The use of NSAIDs in the early post-injection
period may exert an inhibitory effect on healing, and the use of local anaesthesia
13
at the injection site is controversial . Extra-articular injections are performed
under ultrasound guidance, and it is suggested that the haematoma, if present,
should be evacuated and replaced with PRP.

Oversimplification:

Over this background, the sceptics point out that, given the well concerted
healing cascade which has evolved over millions of years, it is not easy to
understand how a single or even a few injections of a cocktail of growth factors at
variable, and at present not well codified, times from the injury will produce a
lasting beneficial effect on a wide variety of condition.

The aim of PRP injections is to achieve predictable and fast tissue repair through
a new well-organized extracellular matrix, which ideally would reach the high
mechanical performance and functional levels of native tissue in the shortest time
possible. Despite the hype of the technique and its biological plausibility, the
anecdotal nearly miraculous recovery reported in the lay press in some famous
athletes, and the myriad of extremely favourable retrospective and prospective
studies published, level I investigations are lacking: we prompt researchers to
undertake appropriately powered level I studies with adequate and relevant
outcome measures and clinically appropriate follow up.

Copyright

The Corresponding Author has the right to grant on behalf of all authors and
does grant on behalf of all authors, an exclusive licence (or non exclusive for
government employees) on a worldwide basis to the BMJ Publishing Group Ltd, and
its Licensees to permit this article (if accepted) to be published in BMJ editions and
any other BMJPGL products and to exploit all subsidiary rights, as set out in our
licence (bmj.com/advice/copyright.shtml).”

Competing interest statement

All authors declare that the answer to the questions on your competing
interest form are all No and therefore have nothing to declare

Competing interests
None declared.

References:
1. Marx, R.E. Platelet-rich plasma (PRP): What is PRP and what is not PRP?
Implant Dent 10, 225, 2001.
2. Dohan Ehrenfest DM, Rasmusson L, Albrektsson T. Classification of platelet
concentrates: from pure platelet-rich plasma (P-PRP) to leucocyte- and
platelet-rich fibrin (L-PRF). Trends Biotechnol. 2009;27(3):158-67.
3. Sánchez M, Anitua E, Orive G, Mujika I, Andia I. Platelet-rich therapies in
the treatment of orthopaedic sport injuries. Sports Med. 2009;39(5):345-
54.
4. Mazzucco L, Balbo V, Cattana E, Guaschino R, Borzini P. Not every PRP-gel
is born equal. Evaluation of growth factor availability for tissues through
four PRP-gel preparations: Fibrinet, RegenPRP-Kit, Plateltex and one manual
procedure. Vox Sang. 2009;97(2):110-8.
5. Anitua E, Sanchez M, Nurden AT, Nurden P, Orive G, Andia I. New insights
into and novel applications for platelet-rich fibrin therapies. Trends
Biotechnol. 2006;24(5):227-34.
6. Graziani F, Ivanovski S, Cei S, Ducci F, Tonetti M, Gabriele M. The in vitro
effect of different PRP concentrations on osteoblasts and fibroblasts. Clin
Oral Implants Res. 2006;17(2):212-9.
7. Weibrich G, Hansen T, Kleis W, Buch R, Hitzler WE. Effect of platelet
concentration in platelet-rich plasma on peri-implant bone regeneration.
Bone. 2004;34(4):665-71.
8. Marx, RE. Platelet-rich plasma: evidence to support its use. J Oral Maxillofac
Surg 62, 489, 2004.
9. Weibrich G, Kleis WK, Hafner G, Hitzler WE. Growth factor levels in platelet-
rich plasma and correlations with donor age, sex, and platelet count. J
Craniomaxillofac Surg. 2002;30(2):97-102.
10. Tidball JG. Inflammatory processes in muscle injury and repair. Am J
Physiol Regul Integr Comp Physiol. 2005;288(2):R345-53.
11. Asfaha S, Cenac N, Houle S, Altier C, Papez MD, Nguyen C, Steinhoff M,
Chapman K, Zamponi GW, Vergnolle N. Protease-activated receptor-4: a
novel mechanism of inflammatory pain modulation. Br J Pharmacol.
2007;150(2):176-85.
12. Everts PA, Devilee RJ, Brown Mahoney C, van Erp A, Oosterbos CJ,
Stellenboom M, Knape JT, van Zundert A. Exogenous application of platelet-
leukocyte gel during open subacromial decompression contributes to
improved patient outcome. A prospective randomized double-blind study.
Eur Surg Res. 2008;40(2):203-10.
13. Sampson S, Gerhardt M, Mandelbaum B. Platelet rich plasma injection
grafts for musculoskeletal injuries: a review. Curr Rev Musculoskelet Med.
2008;1(3-4):165-74.
14. Sanchez M, Anitua E, Azofra J, Andia I, Padilla S, Mujika I. Comparison of
surgically repaired achilles tendon tears using platelet-rich fibrin matrices.
Am J Sports Med. 2007;35(2):245-51.
15. Eppley BL, Woodell JE, Higgins J.Platelet quantification and growth factor
analysis from platelet-rich plasma: implications for wound healing. Plast
Reconstr Surg. 2004;114(6):1502-8.
16. Akeda K, An HS, Okuma M, Attawia M, Miyamoto K, Thonar EJ, Lenz ME,
Sah RL, Masuda K. Platelet-rich plasma stimulates porcine articular
chondrocyte proliferation and matrix biosynthesis. Osteoarthritis Cartilage.
2006;14(12):1272-80.
17. Ishida K, Kuroda R, Miwa M, Tabata Y, Hokugo A, Kawamoto T, Sasaki K,
Doita M, Kurosaka M.The regenerative effects of platelet-rich plasma on
meniscal cells in vitro and its in vivo application with biodegradable gelatin
hydrogel. Tissue Eng. 2007;13(5):1103-12.
18. Wright-Carpenter T, Klein P, Schäferhoff P, Appell HJ, Mir LM, Wehling P.
Treatment of muscle injuries by local administration of autologous
conditioned serum: a pilot study on sportsmen with muscle strains. Int J
Sports Med. 2004;25(8):588-93.
19. Hammond JW, Hinton RY, Curl LA, Muriel JM, Lovering RM. Use of
autologous platelet-rich plasma to treat muscle strain injuries. Am J Sports
Med. 2009;37(6):1135-42.
20. Sánchez M, Anitua E, Azofra J, Aguirre JJ, Andia I. Intra-articular injection
of an autologous preparation rich in growth factors for the treatment of
knee OA: a retrospective cohort study. Clin Exp Rheumatol.
2008;26(5):910-3.
21. Everts PA, Devilee RJ, Oosterbos CJ, Mahoney CB, Schattenkerk ME, Knape
JT, van Zundert A. Autologous platelet gel and fibrin sealant enhance the
efficacy of total knee arthroplasty: improved range of motion, decreased
length of stay and a reduced incidence of arthrofibrosis. Knee Surg Sports
Traumatol Arthrosc. 2007;15(7):888-94.
22. Kawasumi M, Kitoh H, Siwicka KA, Ishiguro N. The effect of the platelet
concentration in platelet-rich plasma gel on the regeneration of bone. J
Bone Joint Surg Br. 2008;90(7):966-72.
23. Murray MM, Spindler KP, Devin C, Snyder BS, Muller J, Takahashi M,
Ballard P, Nanney LB, Zurakowski D. Use of a collagen-platelet rich plasma
scaffold to stimulate healing of a central defect in the canine ACL. J Orthop
Res. 2006;24(4):820-30.
24. Fleming BC, Spindler KP, Palmer MP, Magarian EM, Murray MM. Collagen-
platelet composites improve the biomechanical properties of healing
anterior cruciate ligament grafts in a porcine model. Am J Sports Med.
2009;37(8):1554-63.
25. Mishra A, Pavelko T. Treatment of chronic elbow tendinosis with buffered
platelet-rich plasma. Am J Sports Med. 2006;34(11):1774-8.
26. Nagae M, Ikeda T, Mikami Y, Hase H, Ozawa H, Matsuda K, Sakamoto H,
Tabata Y, Kawata M, Kubo T. Intervertebral disc regeneration using platelet-
rich plasma and biodegradable gelatin hydrogel microspheres. Tissue Eng.
2007;13(1):147-58.
27. Hamilton B, Grantham J, Chalabi H. Use of complex growth factor
preparations in the manegment of muscle strain injury. Aspetar Consensus.
QATAR. 2008.
28. Creaney L, Hamilton B. Growth factor delivery methods in the management
of sports injuries: the state of play. Br J Sports Med. 2008;42(5):314-20.
29. Banfi G, Corsi MM, Volpi P. Could platelet rich plasma have effects on
systemic circulating growth factors and cytokine release in orthopaedic
applications? Br J Sports Med. 2006;40(10):816.


SELECTED ABSTRACTS FROM SPORTS INJURY
LITERATURE AND RELATED ISSUES

Dr. Ronen Debi *


* Chairmen of the Dept. of Orthopaedics in Barzilay Hospital, Ashkelon, ISRAEL

Three-Dimensional Kinematic and Kinetic Analysis of Knee Rotational


Stability After Single- and Double-Bundle Anterior Cruciate Ligament
Reconstruction

Tsarouhas A, Iosifidis M, Kotzamitelos D, Spyropoulos G, Tsatalas T, Giakas G. Three-


Dimensional Kinematic and Kinetic Analysis of Knee Rotational Stability After Single- and
Double-Bundle Anterior Cruciate Ligament Reconstruction. Arthroscopy: The Journal of
Arthroscopic and Related Surgery July 2010: 26(7);869-1010

Objective. To investigate whether anatomic restoration of the anterior cruciate


ligament (ACL) functional bundles results in significant reduction in transverse-
plane instability compared with the conventional single-bundle technique during a
dynamic 60° pivoting maneuver with the supporting knee in extension

Methods. Using an 8-camera optoelectronic system and a force plate, we


examined 10 patients with double-bundle ACL reconstruction, 12 patients with
single-bundle reconstruction, 10 ACL-deficient subjects, and 10 healthy control
individuals. The 4 groups did not differ in terms of age, body mass index, duration
of follow-up, and number of meniscectomies performed. Kinematic and kinetic data
were collected from these subjects while performing a pivoting maneuver on each
side with the supporting knee in extension. Maximum range of motion for internal-
external knee rotation and maximum knee rotational moment were examined.

Results. There was no significant difference in tibial rotation either between the 4
groups or between sides. The mean knee rotation for the single- and double-
bundle groups was lower than the control group. Rotational moment values were
substantially reduced on the affected side of the reconstructed and the ACL-
deficient groups. However, rotational moment was not found to affect the degree
of angular displacement significantly.

Conclusion. Double-bundle ACL reconstruction does not reduce knee rotation


further compared with the single-bundle reconstruction technique. The affected
side of ACL-deficient or -reconstructed individuals is subjected to reduced knee
rotational moments compared with the intact side during stressful functional
maneuvers.

Is the Outcome of Caudal Epidural Injections Affected by Patient


Positioning?

Makki D, Nawabi DH, Francis R, Hamed AR, Hussein AA. Is the Outcome of Caudal
Epidural Injections Affected by Patient Positioning? Spine. 35(15):E687-E690, July
1, 2010.

Objective. To investigate the effect of the lateral decubitus position, after a caudal
epidural injection, on outcome.

Caudal epidural injections are used widely in the treatment of low back pain and
radicular leg pain. Various measures have been used to improve the efficacy of
these injections in previous studies. Our aim was to investigate the effect of the
lateral decubitus position, after administering a caudal epidural injection, on
outcome.

Methods. Fifty-seven patients undergoing caudal epidural injection for low back
pain associated with radicular leg pain were randomly allocated into 2 groups.
Group 1 (treatment group) had 28 patients who were placed in the lateral
decubitus position after injection. Group 2 (control group) had 29 patients who
were laid supine after injection. Patients were assessed before injection using the
Verbal Pain Score (VPS) and the Oswestry Disability Index (ODI). They were
reassessed after 6 weeks using the same outcome measures.

Results. Both groups demonstrated improvement after injection. The degree of


improvement in the VPS was significantly greater in group 1 compared with group
2 (P = 0.00007). The degree of improvement in the ODI was not statistically
significant (P = 0.14).

Conclusion. Laying a patient on the side of their leg pain after a caudal epidural
injection has a beneficial effect on the degree of pain relief. We recommend that
this simple and safe maneuver be introduced routinely after administering a caudal
epidural injection, to aid in the eventual outcome of a potentially difficult clinical
problem.

Life Quality After Instrumented Lumbar Fusion in the Elderly

Becker P, Bretschneider W, Tuschel A, Ogon M. Life Quality After Instrumented


Lumbar Fusion in the Elderly.Spine. 35(15):1478-1481, July 1, 2010.

Objective. To review the clinical outcome on elderly patients after spinal


instrumented fusion.

Although lumbar fusion in elderly patients has increased rapidly, there are only few
and conflicting results regarding the clinical outcome.

Methods. This retrospective review evaluated 195 patients aged 70 to 89 who


underwent lumbar spinal fusion. All 195 patients had follow-ups after 6 weeks, 1
year, and 2 years, including clinical evaluation as well as visual analog scale score,
Oswestry Disability Index, and Short Form health survey.

Results. Elderly patients benefit from spinal fusion. Back and leg pains were
initially reduced by >50%, with a slight deterioration over a 2-year period. Pain
medication was reduced in 69% of the patients, and 89.7% of the patients were
satisfied.

Conclusion. Age itself cannot be considered a contraindication.


Sex Differences in Patient-Reported Outcomes After Anterior Cruciate
Ligament Reconstruction

Ageberg E, Forssblad M, Herbertsson P, Roos EM. Sex Differences in Patient-


Reported Outcomes After Anterior Cruciate Ligament Reconstruction: Data From
the Swedish Knee Ligament Register. Am J Sports Med July 2010; 38:1334-1342

Background: Female gender is a risk factor for sustaining anterior cruciate


ligament (ACL) injury. However, little is known about possible sex differences in
patients with ACL injury/reconstruction.

Objective: To study sex differences in patient-reported outcomes before and at 1


and 2 years after ACL reconstruction and to present reference values.

Methods: Between 2005 and 2008, 10164 patients (mean age, 27 years; SD, 9.8;
42% females) with primary ACL reconstruction were registered in the Swedish
national knee ligament register. There were 4438 (44%) of these patients (42%
females) who had completed the knee-specific questionnaire, Knee injury and
Osteoarthritis Outcome Score (KOOS), and 5255 (52%) who had completed the
generic score of health status, EQ-5D, before surgery and were included in this
study. Independent t tests were used to study sex differences in KOOS and EQ-5D
preoperatively, 1 and 2 years postoperatively, and over time.

Results: Preoperatively, female patients reported worse scores than male patients
in 4 KOOS subscales (pain, symptoms, sport/recreation, quality of life) and EQ-5D,
with the largest difference seen in KOOS sport/recreation (mean difference, 4.7;
95% confidence interval [CI], 3.0-6.3). At 1 year postoperatively, female patients
reported worse scores than male patients in KOOS pain (mean difference, 1.4;
95% CI, 0.4-2.4) and KOOS sport/recreation (mean difference, 2.7; 95% CI, 0.9-
4.4) and at 2 years postoperatively in KOOS sport/recreation (mean difference,
4.4; 95% CI, 2.1-6.7) and KOOS quality of life (mean difference, 2.4; 95% CI,
0.4-4.4). Female patients reported less improvement from 1 to 2 years
postoperatively than male patients in KOOS sport/recreation (mean difference,
3.2; 95% CI, 0.3-6.1). In some age groups, female patients reported a clinically
relevant worse KOOS sport/recreation score than male patients (mean difference
≥8).
Conclusion: Female patients reported statistically significant worse outcomes than
male patients before and at 1 and 2 years after ACL reconstruction. In some age
groups, this difference was also clinically relevant. There were no clinically relevant
sex differences in improvements over time. We suggest that possible sex
differences be analyzed in future studies on evaluation after ACL
injury/reconstruction.

Biomechanical Comparisons of Knee Stability After Anterior Cruciate


Ligament Reconstruction Between 2 Clinically Available Transtibial
Procedures: Anatomic Double Bundle Versus Single Bundle

Kondo E, Merican AM, Yasuda K, Amis AA. Biomechanical Comparisons of Knee


Stability After Anterior Cruciate Ligament Reconstruction Between 2 Clinically
Available Transtibial Procedures: Anatomic Double Bundle Versus Single Bundle
Am J Sports Med July 2010 38:1349-1358

Background: Several trials have compared the clinical results between anatomic
double-bundle and single-bundle anterior cruciate ligament reconstruction
procedures. However, it remains controversial whether the anatomic double-bundle
procedure is superior to the single-bundle procedure.

The anatomic double-bundle procedure will be better than the single-bundle


procedure at resisting anterior laxity, internal rotation laxity, and pivot-shift
instability.

Methods: Eight cadaveric knees were tested in a 6 degrees of freedom rig using
the following loading conditions: 90-N anterior tibialforce, 5-N—m internal and
external tibial torques, and a simulated pivot-shift test. Tibiofemoral kinematics
during the flexion-extension cycle were recorded with an optical tracking system
for (1) intact, (2) anterior cruciate ligament–deficient knee, (3) anatomic double-
bundle reconstruction, and (4) single-bundle reconstruction placed at 11 o’clock in
the intercondylar notch.
Results: There were significant reductions of anterior laxity of 3.5 mm at 20° of
flexion, internal rotational laxity of 2.5° at 20° of flexion, and anterior translations
(2 mm) and internal rotations (5°) in the simulated pivot-shift test in the double-
bundle reconstruction com-pared with the single-bundle reconstruction. There were
no significant differences between the 2 procedures for external rotation laxity.

Conclusion: The postoperative anterior translation and internal rotation stability


after anatomic double-bundle anterior cruciate ligament reconstruction were
significantly better than after single-bundle reconstruction, in both static tests and
the pivot shift.

Modified Impingement Test Can Predict the Level of Pain Reduction After
Rotator Cuff Repair

Joo Han O, Sae Hoon K, Kyung Hwan K, Chung Hee O, Hyun Sik G. Modified
Impingement Test Can Predict the Level of Pain Reduction After Rotator Cuff
Repair. Am J Sports Med July 2010 38:1383-1388

Background: Most patients experience a significant reduction in pain after rotator


cuff repair. However, there is currently no method to predict the level of pain
reduction that each patient will experience. This report explores the usefulness of
the modified impingement test for prognosis in cases of rotator cuff repair.

The amount of pain reduction after injection of lidocaine into the subacromial space
preoperatively correlates with the level of pain reduction after rotator cuff repair.

Methods: Preoperatively, a visual analog scale for pain was measured in 153
patients (59 males and 94 females) with a rotator cuff tear before and after
injection of lidocaine into the subacromial space. Subsequently, rotator cuff repair
was performed. At least 1 year after surgery, the visual analog scale for pain and
satisfaction, Constant score, Simple Shoulder Test, American Shoulder and Elbow
Surgeons (ASES) score, and University of California, Los Angeles shoulder rating
scale were evaluated. Correlation analyses were performed between the change in
visual analog scale after the modified impingement test and after surgery.

Results: The amount of pain reduction after the modified impingement test was
significantly related to improvement of pain postoperatively (P < .001), as
measured using the visual analog scale for pain. The change in ASES score was
also related to the amount of pain reduction after the modified impingement test (P
= .001); however, the other tests showed no statistical significance (P > .05).
Univariate regression analysis revealed that a 0.621-unit reduction in postoperative
pain on the visual analog scale could be expected for each 1 unit (on a scale of 10)
reduction in pain after lidocaine injection preoperatively.

Conclusion: The amount of pain reduction after the modified impingement test
preoperatively correlated with the improvement of pain after rotator cuff repair.
This simple preoperative test could help patients understand the subjective level of
pain reduction that they may experience after rotator cuff repair.

Chondral Resurfacing and High Tibial Osteotomy in the Varus Knee:


Survivorship Analysis

William I. Sterett WI, Steadman JR, Huang MJ, Matheny LM, Briggs KK. Chondral
Resurfacing and High Tibial Osteotomy in the Varus Knee: Survivorship Analysis.
Am J Sports Med July 2010 38:1420-1424

Active patients with arthritic malalignment of the knee are difficult to manage.
Arthroplasty, unicompartmental or total knee replacement, may not be appropriate
in patients who desire to remain highly active. High tibial osteotomy has been
recommended for the treatment of varus osteoarthritis to decrease pressure on the
damaged medial compartment.

Objective: To determine the length of time patients with varus gonarthrosis can
avoid knee arthroplasty with chondral resurfacing (microfracture) and medial
opening wedge high tibial osteotomy (HTO).
Methods: From 1995 to 2001, the senior authors performed a medial opening
wedge HTO/microfracture in 106 knees (mean age, 52 years; range, 30-71 years).
Survivorship was defined as not requiring knee arthroplasty after microfracture and
HTO.

Results: At 5 years, survivorship was 97%. At 7 years, survivorship was 91%.


Twelve patients proceeded to arthroplasty at a mean of 81 months (range, 19-116
months). Follow-up was obtained for 90% of patients. At most recent follow-up,
the mean Lysholm score was 71 (range, 5-100). At 3 years, the mean Lysholm
score was 73, Tegner score was 2.8, and patient satisfaction was 7.9. At 5 years,
the mean Lysholm score was 73, Tegner score was 3.8, and patient satisfaction
was 7.5. At 9 years, the mean Lysholm score was 67, Tegner score was 3.1, and
patient satisfaction was 7.5. Patients with medial meniscus injury at surgery were
9.2 times more likely to undergo arthroplasty than patients without (95%
confidence interval [CI], 1.4-13.5; P = .015).

Conclusion: With 91% survivorship at 7 years, microfracture/HTO seems to


contribute to a delay of knee replacement in active patients with varus
gonarthrosis. Patients who proceeded to knee arthroplasty after combined
HTO/microfracture had a mean delay of 81.3 months.

Generalized Joint Hypermobility and Risk of Lower Limb Joint Injury


During Sport: A Systematic Review With Meta-Analysis

Pacey V, Nicholson LL, Adams RD, Munn J, Munns CF. Generalized Joint
Hypermobility and Risk of Lower Limb Joint Injury During Sport, A Systematic
Review With Meta-Analysis. Am J Sports Med July 2010 38:1487-1497

Generalized joint hypermobility is a highly prevalent condition commonly


associated with joint injuries. The current literature has conflicting reports of the
risk of joint injury in hypermobile sporting participants compared with their
nonhypermobile peers. Systematic reviews have not been conclusive and no meta-
analysis has been performed.
Objective: This review was undertaken to determine whether individuals with
generalized joint hypermobility have an increased risk of lower limb joint injury
when undertaking sporting activities.

Study Design: Systematic review with meta-analysis.

Methods: Studies were identified through a search without language restrictions


of PubMed, CINAHL, Embase, and SportDiscus databases from the earliest date
through February 2009 with subsequent handsearching of reference lists. Inclusion
criteria for studies were determined before searching and all included studies
underwent methodological quality assessment by 2 independent reviewers. Meta-
analyses for joint injury of the lower limb, knee, and ankle were performed using a
random effects model. The difference in injury proportions between hypermobility
categories was tested with the z statistic.

Results: Of 4841 identified studies, 18 met all inclusion criteria with


methodological quality ranging from 1 of 6 to 5 of 6. A variety of tests of
hypermobility and varied cutoff points to define the presence of generalized joint
hypermobility were used, so the authors determined a standardized cutoff to
indicate generalized joint hypermobility. Using this criterion, a significantly
increased risk of knee joint injury for hypermobile and extremely hypermobile
participants compared with their nonhypermobile peers was demonstrated (P <
.001), whereas no increased risk was found for ankle joint injury. For knee joint
injury, a combined odds ratio of 4.69 (95% confidence interval, 1.33-16.52; P =
.02) was calculated, indicating a significantly increased risk for hypermobile
participants playing contact sports.

Conclusion: Sport participants with generalized joint hypermobility have an


increased risk of knee joint injury during contact activities but have no altered risk
of ankle joint injury.
Resurfacing arthroplasty of the hip for avascular necrosis of the femoral
head

Bose VC, Baruah BD. Resurfacing arthroplasty of the hip for avascular necrosis of
the femoral head: A Minimum follow-up of four years. J Bone Joint Surg Br 2010
92-B: 922-928

We performed 96 Birmingham resurfacing arthroplasties of the hip in 71


consecutive patients with avascular necrosis of the femoral head.

Methods: A modified neck-capsule-preserving approach was used which is


described in detail. The University of California, Los Angeles outcome score, the
radiological parameters and survival rates were assessed.

Results: The mean follow-up was for 5.4 years (4.0 to 8.1). All the patients
remained active with a mean University of California, Los Angeles activity score of
6.86 (6 to 9). Three hips failed, giving a cumulative survival rate of 95.4%. With
failure of the femoral component as the endpoint, the cumulative survival rate was
98.0%. We also describe the combined abduction-valgus angle of the bearing
couple, which is the sum of the inclination angle of the acetabular component and
the stem-shaft angle, as an index of the optimum positioning of the components in
the coronal plane.

Conclusions: Using a modified surgical technique, it is possible to preserve the


femoral head in avascular necrosis by performing hip resurfacing in patients with
good results.
Injury to the proximal deep medial collateral ligament

Narvani A, Mahmud T, Lavelle J, Williams A. Injury to the proximal deep medial


collateral ligament: A Problematical subgroup of injuries. J Bone Joint Surg Br
2010 92-B: 949-953

Most injuries to the medial collateral ligament (MCL) heal well after conservative
treatment. We have identified a subgroup of injuries to the deep portion of the MCL
which is refractory to conservative treatment and causes persistant symptoms.
They usually occur in high-level football players and may require surgical repair.

Methods: We describe a consecutive series of 17 men with a mean age of 29


years (18 to 44) who were all engaged in high levels of sport. Following a minor
injury to the MCL there was persistent tenderness at the site of the proximal
attachment of the deep MCL. It could be precipitated by rapid external rotation at
the knee by clinical testing or during sport.

Results: The mean time from injury to presentation was 23.6 weeks (10 to 79)
and none of the patients had responded to conservative treatment. The surgical
finding was a failure of healing of a tear of the deep MCL at its femoral origin which
could be repaired. After a period of postoperative protective bracing and
subsequent rehabilitation the outcome was good. All the patients returned to their
sports and remained asymptomatic at a mean of 48 weeks (28 to 60) post-
operatively.

Conclusions: Recognition of this subgroup is important since the clinical features,


the course of recovery and surgical requirement differ from those of most injuries
to the MCL.


Mountain Biking Injuries: Current Concepts

Mike Carmont

Mountain biking has now developed as a recreational adventure pastime to a


professional competitive sport with a World Cup Series, World Championships and
Olympic competitions.

Research has shown that the downhill form of racing has a significantly higher
injury rate (4.34 per 100 hours riding) than X country racing (0.37 per 100hrs) and
injured riders are typically male aged 20-39 years.

Falls over the handlebars have a more severe injury profile with exposure to head,
face and cervical spine injuries. Falls to the side tend to result in lower limb
injuries. The majority of riders injured will have sustained soft tissue injuries such
as abrasions and contusions and the commonest fracture is the clavicle,
commonest dislocation is the ACJ.

Education campaigns have led to a reduction of head injuries with helmet use,
abdominal injuries with the avoidance of bar ends and the use of a face mask is
recommended to reduce facial injury.

Mountain biking is a fast fun adventure sport, which cannot be learnt for books or
in the classroom. Riders are recommended to race within the level of their
capability although the risk of injury adds to the excitement.

© 2010 EFOST
www.efost.org


FUTURE COURSES & MEETINGS
1 October 2010 2010 Korea Arthroscopy Society Seoul, South Korea www.korarthro.com

Annual Meeting With Arthroscopy


Master of ASIA
1-2 October 2010 AOFAS Complete Foot Care Course Pennsylvania, USA http://www.aofas.org/Scripts/4Disapi.dll/4
DCGI/events/47.html?Action=Conference_
Detail&ConfID_W=47
th www.severanscopy.com
2 October 2010 46 Shoulder Severance Arthroscopy Seoul, South Korea
Fresh Cadever Workshops
7-8 October 2010 Ukrainian Congress of Arthroscopy, Kiev, Ukraine www.uastka.org

Knee Surgery and Sport Trauma


7-9 October 2010 4nd Advanced Course on Knee Lyon, France http://www.lyon-genou.com

Arthroplasty – 14èmes Journées


Lyonnaises de Chirurgie du Genou
th http://www.tusyad2010.org/eng
12-16 October 2010 10 Turkish Sports Traumatology Antalya, Turkey
Arthroscopy and Knee Surgery
Congress
14-16 October 2010 Orthopedic Surgery Controversies Napa, USA www.orthopedicsurgerycontroversies.com

2010
14 October 2010 London Knee Meeting London, England http://www.londonkneemeeting.co.uk/

20 October 2010 The 2nd Israeli Congress for Tel Aviv, Israel www.medicalmedia.co.il/osteo-arth

Osteoarthritis
20-22 October 2010 International Congress on External Barcelona, Spain www.externalfixation2010.com

Fixation & Bone Reconstruction


11 November 2010 Gijon Knee Sports Meeting 2010 Gijon, Spain http://www.gks2010.com/inicio.html

25-27 November 2010 6th EFOST Meeting Brussels, Belgium www.efost2010.org

1-4 December 2010 SFA annual congress Aix en Provence , http://www.sofarthro.org

France
2-4 December 2010 Basic & Advanced Knee Arthroscopy Cairo, Egypt www.lrc.edu.eg

Basic Shoulder Arthroscopy


9 December 2010 Advanced Team Physician Course Washington, USA
http://www.sportsmed.org/tabs/education
/meetingDetails.aspx?EID=83
10 December 2010 Anti Doping and Knee Injuries London, England
http://www.djoglobal.eu/en_UK/DJO_Educ
ation_Events.html
13-15 January 2011 FIVB Volleyball Medicine Congress Bled, Slovenia www.fivbmedicine2011.org

2011
26-27 January 2011 27th International Jerusalem Jerusalem, Israel jerusalemsymposium@regin-med.co.il

Symposium on Sports Medicine


15-19 February 2011 The AAOS 2011 Annual Meeting San Diego, USA http://www.aaos.org/education/anmeet/a
nmeet.asp
3-5 April 2011 IOC Advanced Team Physician Course Corsica
7-9 April 2011 International Olympic Committee Monte Carlo, www.ioc-preventionconference.org

Monaco
14-17 April 2011 30th AANA Annual Meeting San Francisco, USA http://www.aana.org/Home/tabid/36/Defa
ult.aspx
15-19 May 2011 8th Biennial ISAKOS Congress Rio de Janeiro, isakos@isakos.com

Brazil
th http://www.aoassn.org/index.asp
22-25 June 2011 124 AOA Annual Meeting Boston, MA, USA
14-17 September 2011 European Society for Surgery of the Lyon, France www.mcocongres.com

Shoulder and the Elbow


4-9 October 2011 22th Turkish National Orthopaedics Antalya, Turkey http://www.totbid.org.tr/

& Traumatolgy Congress


th http://esska-
1-5 May 2012 15 ESSKA Congress Geneva,
congress.org/esska2012/index.html
Switzerland
7-10 November 2012 World Sport Trauma Congress London, UK www.wstc2012.com

13-16 June 2013 XVIII th FESSH Congress Antalya, Turkey www.fessh.com; gursel@hacettepe.edu.tr
Key Invited Lectures

Knee Ligaments:

• Anatomical ACL Reconstruction – What Have We Learned?


• Technique and Results of PCL Inlay Reconstruction
• Concept and Technique of Treatment in Knee Dislocation
• Arthroscopic Treatment of Tibia plateau fracture
• Primary Repair Combined with Bone Marrow Stimulation in Acute ACL
Lesions: Results in a group of athletes at 3 year follow up
• Single versus Double bundle technique in ACL reconstruction using the
Semitendinosus Tendon
• Principles of Revision ACL reconstruction
• ACL tears: to reconstruct or augment
• Algorithm Based ACL Reconstruction: Graft Choice and Technique
• Current Treatment Options for PCL Injuries
• ACL reconstruction with one hamstring: all inside technique

Cartilage

• Mesenchymal Stem Cells Implantation for Full-Thickness Cartilage Lesions


Treatment: Results at 2 year follow up

Subjects of Interest

• Arthroscopic Treatment of Tibia plateau fracture


• Infiltrative Treatment with Autologous Platelet Rich Plasma (P.R.P.) in early
Osteoarthritis: Results at 12 month follow up
• Distraction arthroplasty: a new surgical technique for the treatment of basal
thumb
• Osteotomies About the Knee: Joint Preservation and Osteoarthritis
• Neuromuscular control and exercise-related leg pain in triathletes
General Sports

• Predictive Factors for a Safe Return-to-sport


• The Identification and Treatment of Eating Disorders Among Elite Athletes
• Child Neurodevelopment and Sports Participation
• Medical Disorders and Sports Participation by Children and Adolescents
• Concussion in Pediatric Sports: Current Issues

Imaging

• Ergonomic Factors by Radiology.


• Muscle Injuries
• Post operative imaging of the knee.
• Finger injuries

Knee Meniscus

• Meniscal repair: when to repair and technique


• Meniscal Tears: Repair, Resect, Replace?

Upper Limp
• Massive Rotator Cuff Tears: A Case-Based Approach
• Shoulder Instability: Posterior-MDI Treatment Options
• Lateral elbow tendinopathy – Examination and treatment - what you always
wanted to know…………
• Optimising corticosteroid injection for lateral elbow tendinopathy with the
addition of physiotherapy

Anterior Knee Pain

• "Put your foot in it" - orthoses in the management of anterior knee pain.
• Predictors of short and long term outcome in patellofemoral pain syndrome
• Targeted physiotherapy for patellofemoral joint osteoarthritis

Foot and Ankle

• Modified Watson-Jones technique for chronic lateral ankle instability in athletes.


© 2010 EFOST
www.efost.org
EFOST 2012

WORLD SPORTS TRAUMA CONGRESS 2012

These events are being combined in a meeting to be held in London, the host city
for the 2012 Olympic games. The venue is likely to be the Queen Elizabeth 2nd
Conference centre, which is in the heart of the city of London. All the major
attractions of this magnificent city are in easy reach of this top class centre. The
meeting will be held in early November 2012. The meeting will run over 4 days.
We are pleased to have the support of the BOA (British Orthopaedic Association),
the BOA (British Olympic Association) doctors group, the new Faculty for Sport and
Exercise Medicine, and the British Association for Sport and Exercise Medicine. We
will be including an Allied Health professionals programme. The specialist societies
of the BOA (Orthopaedic) have been invited to run programmes within the
meeting. This promises to be a top class academic meeting with the opportunity to
experience all of the unique sight-seeing wonders of London. Put it in your calendar
now!

Roger Hackney

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© 2010 EFOST
Product information: brief summary

NAME OF THE MEDICINAL PRODUCT: ChondroCelect 10,000 cells/microlitre implantation


suspension. QUALITATIVE AND QUANTITATIVE COMPOSITION : General description :
Characterized viable autologous cartilage cells expanded ex vivo expressing specific marker
proteins. Qualitative and quantitative composition : Each vial of product contains 4 million
autologous human cartilage cells in 0.4 ml cell suspension, corresponding to a concentration of
10,000 cells/microlitre. PHARMACEUTICAL FORM: Implantation suspension. Before re-
suspension the cells are settled to the bottom of the container forming an off-white layer and the
excipient is a clear colourless liquid. Therapeutic indications: Repair of single symptomatic
cartilage defects of the femoral condyle of the knee (International Cartilage Repair Society [ICRS]
grade III or IV) in adults. Concomitant asymptomatic cartilage lesions (ICRS grade I or II) might be
present. Demonstration of efficacy is based on a randomized controlled trial evaluating the efficacy
of Chondrocelect in patients with lesions between 1-5cm². Posology and method of
administration: ChondroCelect must be administered by an appropriately qualified surgeon and is
restricted to hospital use only. ChondroCelect is solely intended for autologous use and should be
administered in conjunction with debridement (preparation of the defect bed), a physical seal of the
lesion (placement of a biological membrane, preferentially a collagen membrane) and rehabilitation.
Posology: The amount of cells to be administered is dependent on the size (surface in cm²) of the
cartilage defect. Each product contains an individual treatment dose with sufficient number of cells
to treat the pre-defined lesion size, as measured at biopsy procurement. The recommended dose of
ChondroCelect is 0.8 to 1 million cells/cm², corresponding with 80 to 100 microlitre of product/cm²
of defect. Method of administration: ChondroCelect is intended solely for use in autologous cartilage
repair and is administered to patients in an Autologous Chondrocyte Implantation procedure (ACI).
The implantation should be followed by an appropriate rehabilitation schedule for approximately
one year, as recommended by the physician. Contraindications: Hypersensitivity to any of the
excipients or to bovine serum. ChondroCelect must not be used in case of advanced osteoarthritis of
the knee. Undesirable effects: In a randomized, controlled study in the target population, 51
patients were treated with ChondroCelect. In these patients, a periosteal flap was used to secure the
implant. Adverse reactions occurred in 78.4% of the patients over a 36-months postoperative follow-
up period. The most common adverse reactions were arthralgia (47.1%), cartilage hypertrophy
(27.4%), joint crepitation (17.6%) and joint swelling (13.7%). Adverse reactions collected from 370
patients included in a Compassionate Use Program are similar to those reported in the target
population. Most of the reported adverse reactions were expected as related to the open-knee
surgical procedure. The most frequently occurring reactions reported immediately after surgery
include joint swelling, arthralgia and pyrexia. These were generally mild and disappeared in the
weeks following surgery. Adverse reactions of special interest: Arthrofibrosis: In the compassionate
use patients, a higher incidence of arthrofibrosis and decreased joint range of motion was observed
in a subgroup of patients with a patellar lesion (8.2% and 13.1% respectively) compared to non-
patellar lesions (0.6% and 2.6% respectively). Cartilage hypertrophy: In the majority of the 370
patients included in the Compassionate Use Program, a collagen membrane instead of a periosteal
flap was used to seal the defect. According to current literature the incidence of cartilage
hypertrophy can be reduced by using a collagen membrane to cover the lesion site instead of using a
periosteal flap (Gooding et al., 2006; Niemeyer et al., 2008). When a collagen membrane was used
to seal the lesion site after application of ChondroCelect, the incidence of cartilage hypertrophy was
reported to be 1.8% compared to 25% in the randomized, controlled trial alone. Name of the MA
holder: TiGenix NV, Romeinse straat 12/2, B-3001 LEUVEN, Belgium. Product authorization
number: EU/1/09/563/001.
Medicinal product to restricted medical prescription – restricted to hospital use only.
V1_E_091022/mpo

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