[ RESIDENT’S CASE PROBLEM ]

MICHAEL O. HARRIS-LOVE, MPT, DSc, CSCS¹,²š@EI;F>7$I>H7:;H"PT, CPed²

Patellofemoral Knee Pain in an Adult With

Radiographic Osteoarthritis and Human
Immunodeficiency Virus Infection
p to one third of all older adults in the general population have tion, because 50% of individuals with

U radiographic evidence of osteoarthritis (OA) of the knee, and

10% of adults aged 55 or over have mild or moderate disability
as a result.37 These figures are expected to rise as the age of the
United States population advances. Although OA is complex, the basic
underlying impairments center around radiographic signs of pathology,
such as cartilage damage ( joint space narrowing), subchondral
thickening (sclerosis), and new bone formation (osteophytes), along
with the clinical syndrome of knee pain,
morning stiffness, and crepitus. The
TIJK:O:;I?=D0 Resident’s case problem.
T879A=HEKD:0 Kaposi’s sarcoma (KS) is the
most common form of cancer in patients with human
immunodeficiency virus (HIV) infection. Although KS
is often initially asymptomatic, this neoplasm may
progress to affect multiple organ systems, including
structures of the musculoskeletal system, which can
produce symptoms similar to those associated with
common orthopaedic conditions. This resident’s case
problem describes the evaluation and differential diag-
nosis of a 45-year-old male with HIV and KS, referred to
physical therapy with an initial diagnosis of radiographic
osteoarthritis (OA) and patellofemoral pain syndrome
(PFPS) of the left knee. His primary complaint was knee
pain during end range knee flexion.
T:?7=DEI?I0 The history, systems review, and
examination suggested a source of pain of a nonor-
thopaedic origin. Differential examination ruled out
clinical OA, PFPS, ligament/cartilage derangement,
and tendonitis. Avascular necrosis of the medial
femoral condyle was also considered as a possible
radiographic and clinical syndromes of
knee OA must be given distinct atten-
source of pain. Recent blood tests indicated a high
viral load and low CD4 count, which might have
increased susceptibility to opportunistic infections or
KS tumor progression. The patient was referred back
to his physician for additional follow-up. Magnetic res-
onance imaging (MRI) of the knees were consistent
with a systemic inflammatory process such as KS. A
true-cut biopsy was subsequently scheduled, which
confirmed KS lesions at the left knee.
T:?I9KII?ED0 Physical therapists who manage
orthopaedic conditions should be aware of the
disablement that may result from acquired im-
munodeficiency syndrome-related KS. A thorough
joint-specific examination, with a broad differential
diagnosis, should be employed for patients having
known systemic diseases.
TB;L;BE<;L?:;D9;0 Differential diagnosis,
level 4. J Orthop Sports Phys Ther 2009;39(8):612-
617. doi:10.2519/jospt.2009.2961
TA;OMEH:I0 human immunodeficiency virus
(HIV), Kaposi’s sarcoma, knee pain, physical therapy
radiographic knee OA do not have knee
pain or disability. 37 OA does not typi-
cally affect younger persons. However,
secondary OA may develop at any age
when trauma occurs to the articular
cartilage or to the stabilizing soft tis-
sues surrounding the joint.6 Severe
pain, joint deformity, and considerable
morbidity often result from the pro-
gression of radiographic and clinical
knee OA.
Both OA and patellofemoral pain
syndrome (PFPS) may cause knee pain,
and these conditions are exacerbated
by abnormal tibiofemoral or patel-
lofemoral alignment. 13 The syndrome
of PFPS is a common musculoskeletal
condition characterized by peripatel-
lar pain that worsens during kneeling,
squatting, and the use of stairs. 24 PFPS
is often found in those who are physi-
cally active50 and affects females more
often than males.1 The etiology of PFPS
remains unknown. However, anatomic
structures such as muscle, nerve, sub-
chondral bone, synovium, and reti-
naculum have been implicated in this
syndrome.1,50 The symptoms of PFPS
are typically marked by a pernicious
onset and slow progression. 13 The pro-
posed mechanisms of injury include
abnormal patellofemoral alignment

1
Health Systems Specialist, Washington DC VA Medical Center, Research Service/Geriatrics and Extended Care Service, Washington, DC; Assistant Professor, George Washington
University, School of Medicine and Health Sciences, Doctor of Physical Therapy Program, Washington, DC. 2 Clinical Specialist and Senior Physical Therapist, National Institutes of Health,
Rehabilitation Medicine Department, Physical Therapy Section, Clinical Center, Department of Health and Human Services, Bethesda, MD. The opinions and information contained in this
article are those of the authors and do not necessarily reflect those of the National Institutes of Health or the United States Public Health Service. Address correspondence to Dr Michael
O. Harris-Love, Washington DC VAMC, Research Service/Geriatrics and Extended Care Service, G11, 50 Irving St, NW, Washington, DC 20422. E-mail: michael.harris-love@va.gov

612 | august 2009 | volume 39 | number 8 | journal of orthopaedic & sports physical therapy
and tracking,22 weakness of the quadri-
ceps, predominantly the vastus medialis
obliquus (VMO),23,31 limited hamstring
and iliotibial band flexibility, exces-
sive foot pronation,8,25 and hip muscle
weakness.8,24,40 In addition, PFPS may
be classified as an overuse injury, given
the transient increases in peak pressure
between the patella and femur during
weight-bearing activities such as squat-
ting and kneeling. 9
When a patient with a known sys-
temic disease is referred for examination
of knee pain, clinicians are encouraged
to consider the disease signs and symp-
toms during the differential examination.
Systemic diseases may produce symp-
toms that confound the typical clini-
cal presentation of knee OA and PFPS.
For example, Kaposi’s sarcoma (KS) is a
form of cancer that can affect the lower
extremities and mimic musculoskeletal
symptoms such as painful edema and re-
duced joint range of motion.20 KS is the
most common malignancy associated
with human immunodeficiency virus
(HIV) infection.5 Acquired immunode-
ficiency syndrome (AIDS)-related KS is
a multicentric, inflammatory, angiopro-
liferative lesion that is frequently more
aggressive than the more indolent form
classically seen in elderly males of Medi-
terranean descent. Initial presentation
often includes cutaneous lesions in areas
of skin cleavage of the face and trunk, as
well as the preorbital area, tip of the nose,
gingiva, and external ear.17 An estimated
10% to 24% of individuals with HIV and
AIDS have KS,17 and people with HIV
are 20 000 times more likely to acquire
the neoplastic disorder than the general
population.3 This resident’s case problem
describes the examination, evaluation,
and differential diagnosis of a patient
with HIV seropositivity and AIDS-relat-
ed KS, referred to physical therapy with
an initial diagnosis of radiographic OA
and PFPS of the left knee. We believe it
also highlights the importance of a broad
differential and medical team approach
in the examination of patients with HIV
seropositivity and KS.
journal of orthopaedic & sports physical therapy | volume 39 | number 8 | august 2009 | 613
:?7=DEI?I
FWj_[dj9^WhWYj[h_ij_YiWdZ>_ijeho
T
he patient in this resident’s
case problem was a 45-year-old
Caucasian male diagnosed with
HIV 14 years ago and KS 3 years ago,
both of which were previously managed
at other health care facilities. His chief
complaint was intermittent pain of grad-
ual onset at the posteromedial aspect of
the left knee during gardening activities
that required kneeling. The pain had
been present for 6 weeks. Past medical
history included bipolar disorder, hyper-
tension, hypogonadism, herpes simplex
virus-1, and an undiagnosed left knee
injury due to a skiing accident 7 years
ago. There was no history of knee sur-
gery or recent trauma. A recent radio-
graphic imaging report detailed medial
compartment joint space narrowing and
mediolateral osteophyte formation at
the femoral condyles bilaterally. Four
months before the examination, his CD4
count (a measure of immune system
strength) and viral load values (HIV cells
in the blood) were 212 cells per μL and
1691 RNA copies per mL, respectively,
indicating relatively poor control of his
HIV disease. The patient was undergo-
ing a regimen of HAART (highly active
antiretroviral therapy), that included
the HIV protease inhibitors, Fortovase
(Hoffman-La Roche, Inc, Nutley, NJ)
(saquinavir) and Norvir (Hoffman-La
Roche, Inc) (ritonavir). By inhibiting
HIV protease, these medications block
the enzymatic functions needed for suc-
cessful formation of mature infectious
virus particles.46
The patient did not complain of morn-
ing stiffness or pain after prolonged sit-
ting (the “movie theatre sign”), but he
occasionally experienced severe left knee
pain at rest that woke him from sleep.
Nevertheless, he could ambulate commu-
nity distances and use stairs without knee
discomfort. The patient noted that he did
not engage in any routine exercise regi-
men. His goal was to be able to kneel dur-
ing gardening activities without pain.
<?=KH;'$Cutaneous Kaposi’s sarcoma lesion of the
lower extremities.
F^oi_YWb;nWc_dWj_ed
The systems review led to further exami-
nation of the musculoskeletal, integu-
mentary, and neuromuscular systems.
The patient’s history of HIV and KS, ab-
normal laboratory results (low CD4 and
high viral load), occasional severe pain
at rest, intermittent pain not associated
with walking or squatting, pain-free use
of stairs, and the absence of morning stiff-
ness and movie theatre sign suggested
that systemic disease could be a contrib-
uting factor to his knee pain. However,
the history of previous knee injury, insidi-
ous onset of pain, radiographic presence
of OA, and reports of pain on kneeling
are common signs of PFPS and knee OA
that warranted further examination.
Visual Inspection Visual inspection re-
vealed enlargement of the flexor tendons
at the posteromedial aspect of the left
knee, along with atrophy of the VMO.
Appearance of our patient’s lower ex-
tremities was marked by a sparse distri-
bution of pigmented, well-demarcated
KS lesions, and the left knee was free of
any effusion or discoloration (<?=KH; ').
The KS lesions had been present for 3
years, according to the patient, and had
not changed in shape, size, color, or num-
ber. Manual touch assessment of skin
temperature did not reveal asymmetry, or
apparent elevated temperatures, at either
knee joint.
Girth Measurements Lower extremity
limb girth measurements were taken,
based on the observed atrophy of the left
VMO. The measurements were averaged
from 2 repeated tape measures taken just
 [ RESIDENT’S CASE PROBLEM
proximal to the patella (50 cm proximal
to the lateral malleolus), with the knees
in terminal extension and the patient
supine. The limb girth measurements
were 47 cm on the right and 45 cm on
the left.
Lower Extremity Posture and Align-
ment During inspection and palpation
of postural landmarks, symmetry was
observed for alignment of the patient’s
anterior superior iliac spines in stand-
ing and medial malleoli in supine. Nor-
mal patellar height and orientation and
minimal symmetrical foot pronation was
observed while the patient was standing
barefoot. 32,42 These observations indi-
cated that functional and structural limb
length discrepancy or musculoskeletal
malalignment were not a likely source
of his knee pain. Based on the aforemen-
tioned observations, objective measures
related to limb length were not taken.
Palpation Palpation performed with
the left knee in 90° of flexion did not
produce pain along the medial and lat-
eral tibiofemoral joint lines (sensitivity,
85% to 92%; specificity, 29% to 97%; for
predicting meniscal tears),11,12 patellar
tendon,26 and medial femoral condyle.
However, a verbal pain rating (test-retest
reliability, r = 0.88)15 of 3 to 4 out of a
possible 10 (0, no pain; 10 pain as bad
as it can be) was elicited with palpation
proximal to the adductor tubercle along
the medial border of the VMO.
Special Tests Various tests were used to
assess the ligamentous stability of the
knee. The sensitivity of the Lachman test
to detect rupture of the anterior cruciate
ligament (ACL) is reported to be 80% to
87% for acute injuries and 94% to 99%
for chronic injuries.27,35 The Lachman test
has demonstrated acceptable interrater
reliability,49 based on an intraclass cor-
relation coefficient (ICC2,1) of 0.77 (95%
confidence interval [CI]: 0.50-0.91). Less
is known about the psychometric prop-
erties of varus and valgus stress testing.
Preliminary studies suggest that varus
stress testing has low specificity (25%),19
and valgus stress testing has high speci-
ficity (86% to 96%),16,19 in individuals
614 | august 2009 | volume 39 | number 8 | journal of orthopaedic & sports physical therapy
with ruptured lateral and medial collat-
eral ligaments, respectively. The ligamen-
tous structures of the patient’s knees were
found to be intact upon examination, but
mild laxity was noted on the left with
varus, valgus, and anterior stress testing
(Lachman test).
Other orthopaedic tests at the left
knee included the McMurray test (sen-
sitivity, 29% to 37%; specificity, 77% to
95%), palpation of joint line tenderness
with external/internal rotation of the
tibia (sensitivity, 55% to 85%; specificity,
29% to 67%), and Apley’s test (sensitiv-
ity, 13% to 16%; specificity, 80% to 90%)
to identify a meniscal injury.12,29 Tests
for chondromalacia patella included the
patellar grind test (reliability coefficient,
0.94),7 and the passive patellar tilt test (L
= 0.20-0.35).48 These orthopaedic tests
yielded negative findings, as they did not
provoke any pain. All orthopaedic tests
were administered as described by Magee
(unless otherwise stated).32
Secondary to the lack of positive
test results for orthopaedic knee injury,
further differential screening was per-
formed to rule out the lumbar spine as
a source of the patient’s pattern of pain.
Active and passive lumbar flexion (L =
0.39-0.56), extension (L = 0.29-0.57),
side bending (L = 0.60), and bilateral
rotation (L = 0.10-0.58), performed in
a manner advocated by Saunders et al,41
did not reproduce the patient’s pain.21,33
The quadrant test, straight-leg raise test47
(the patient attained 70° bilaterally; L =
0.68), bowstring test33 (L = 0.11-0.49),
and McKenzie’s side glide test also re-
sulted in negative findings.32,41
Sensation, Range of Motion, and Manual
Muscle Strength Testing Additionally, no
cutaneous sensory impairments at the left
knee, leg, or plantar foot were detected
using Semmes Weinstein monofilament
sensation testing.42 Overpressure during
terminal passive knee flexion produced
pain, located proximal to the adductor
tubercle along the medial border of the
VMO, that was verbally rated as 7 out of
10 by the patient. Active range of motion
(AROM),36 tested via visual observation,
]
and manual muscle testing (MMT)28
were within normal values for the entire
lower quarter. Additionally, when isomet-
ric resistance was applied to the left knee
extensors from a position of 10° short of
full extension, pain was not present.
Gait The patient demonstrated nonan-
talgic, symmetrical step lengths and age-
appropriate gait velocity, based on visual
observation. The patient also exhibited
normal heel strike, transition to flat foot,
and push-off during the examination.
Isokinetic Testing Due to the promi-
nent role of weakness in the syndrome
of patellofemoral joint pain,1,45 and the
inability of MMT to detect 20% to 40%
deficits in strength,2,34 isokinetic testing
of the knee extensors was incorporated
into the examination. The patient com-
pleted 5 repetitions on the Biodex System
2 dynamometer at 60°/s and 180°/s bi-
laterally.38 Patient stabilization and dy-
namometer calibration was performed as
recommended by the manufacturer (Bio-
dex Medical Systems, Inc, Shirley, NY).4
His peak knee extensor torque was 169.1
N·m on the right and 184.3 N·m on the
left at 60°/s, and 157.2 N·m on the right
and 155.4 N·m on the left at 180°/s. Pin-
civero et al38 has demonstrated that the
Biodex System 2 dynamometer is reliable
for knee extensor torque assessment at
similar velocities (ICC2,1 = 0.93-0.97).
;lWbkWj_ed
With the exceptions of pain provocation in
the posteromedial aspect of the knee with
deep palpation and terminal passive flex-
ion of the left knee, no provocative ortho-
paedic test was positive for pain. Isokinetic
and resisted knee extension and flexion
testing ruled out primary muscle impair-
ment. Furthermore, differential screening
of the lumbar spine and musculoskeletal
malalignment did not reveal any findings
suggestive of referred or compensatory
pain patterns. Despite the patient’s radio-
graphic findings of knee OA and refer-
ral diagnosis of PFPS, the pattern of pain
exhibited by the patient was atypical for
PFPS, knee OA, and chronic knee joint in-
stability. “Red flag” findings for a possible
systemic cause of the patient’s left knee
pain included a low CD4 count of only 212
cells per μL and a relatively high viral load
of 1691 RNA copies per mL, along with a
past medical history of KS. A CD4 count of
200 or less is indicative of substantial im-
munodeficiency and an increased risk of
opportunistic infections and tumors (nor-
mal range, 500-1500 cells per μL). The vi-
ral load should normally be undetectable,
and less than 50 RNA copies per mL is the
usual goal of medical treatment. In addi-
tion, the patient’s HIV seropositivity and
intake of protease inhibitors placed him
at risk for avascular necrosis (AVN) of the
medial femoral condyle.39,44 However, the
presence of pain was largely independent of
weight-bearing activity and was inconsis-
tent with common orthopaedic knee pain
syndromes and AVN. The patient’s high
viral load and low CD4 count, along with
the aforementioned examination inconsis-
tencies, led to the suspicion of a systemic
process such as KS, which is beyond the
scope of physical therapy for diagnosis and
management. He was referred back to the
referring physician for further evaluation
on the same day of his physical therapy ex-
amination. The efforts of the medical team
to arrive at a definitive diagnosis based on
the clinical findings and the updated labo-
ratory and imaging results are highlighted
in the next section.
:?I9KII?ED
O
ur patient’s referral diagno-
sis of knee OA and PFPS was not
unsubstantiated, given his initial
clinical presentation of posteromedial
left knee pain during kneeling, quadri-
ceps muscle atrophy, and radiographic
findings of OA. Nevertheless, the clini-
cal and radiographic syndromes of OA
are not always predictive of one another,
and our patient lacked several findings
common to clinical OA. He did not have
joint line tenderness, joint swelling (effu-
sion), crepitus, morning stiffness, or pain
with weight bearing. Despite the patient’s
history of an undiagnosed skiing injury,
which might have been related to the
journal of orthopaedic & sports physical therapy | volume 39 | number 8 | august 2009 | 615
<?=KH;($Coronal and axial MRI views of the lower extremities of our patient. (A) T2-weighted STIR coronal
view showing bilateral abnormal signal intensity at the knee joints and distal aspect of the thighs; (B)
T2-weighted axial section of the distal femur with gadolinium contrast revealing bilateral involvement in a
perineurovascular distribution.
mild asymmetric laxity seen at the left
medial and lateral collateral and anterior
cruciate ligaments, there was no differ-
ence between the radiographic changes
detected at the right and left knees.
The fact that no less than 17 different
clinical signs have been linked to PFPS
confounds its diagnosis.1,45 Despite the
ambiguity of PFPS, key elements of the
patient’s history and examination pro-
vided points of departure from the PFPS
diagnoses. He was a relatively inactive
middle-aged male, with no pain while
descending stairs or rising from a chair.45
He did not exhibit the expected 30% to
40% knee extensor peak torque deficit
with isokinetic strength testing that has
been associated with PFPS.10 Quadriceps
muscle atrophy, a clinical sign associ-
ated with PFPS, was present. However,
the uncommon finding of swelling at the
posteromedial aspect of the left knee was
also observed. A comprehensive group of
objective orthopaedic tests and measures
included in the physical examination
were negative for focal retropatellar in-
jury, muscle length and strength impair-
ments, and lower limb malalignment.
Palpation and other pain-provoking tests
were also negative for tendonitis, OA,
meniscal tear, and significant ligamen-
tous instability.
Differential screening was further
complicated by sequelae secondary to
HIV infection and the side effects of an-
tiretroviral agents, both of which may
result in the development of AVN.18,39,43,44
The development of AVN of the medial
femoral condyle as a complication of HIV
infection has been reported by Stovall
and Young.44 They cite hypertriglyceri-
demia as an important factor in the eti-
ology of AVN due to the associated effect
of cytokines released in response to HIV
infection. The resulting lipid metabolism
dysfunction is thought to play an impor-
tant role in small vessel disease, result-
ing in ischemic necrosis of the affected
region of bone.43,44 Antiretroviral therapy
may play a similar role in the etiology of
AVN, as protease inhibitor-associated
metabolic dysfunction includes dyslipi-
demia.39 Radiographs could have ruled
in asymptomatic AVN of the femoral
condyle; however, reports did not iden-
tify osteonecrosis. Furthermore, the poor
relationship between the patient’s activ-
ity level and symptoms, coupled with his
normal to moderate-range triglyceride
levels (125 to 197 mg/dL over a 6-month
period prior to referral), rendered AVN
subordinate to AIDS-related KS as the
suspected cause of his left knee pain.
This was an important finding because
the patient was being evaluated for in-
vestigational therapy to treat his HIV and
AIDS-related KS.
The medical team ruled out com-
mon orthopaedic conditions as the
source of left knee pain, based on the
patient history and physical exam
findings. Therefore, additional imag-
ing was obtained to investigate the
possibility that the patient’s symp-
toms emanated from systemic disease.
Subsequent T2-weighted STIR mag-
netic resonance images of our patient
( <?=KH; ( ) were notable for abnormal
 [ RESIDENT’S CASE PROBLEM
signal intensity in a perineurovascular
distribution in both lower extremities,
extending from the groin to the mid-
foot. The definitive diagnosis of KS
was determined following a true-cut
biopsy and histopathologic evaluation.
The patient began a scheduled regimen
of recombinant cytokine therapy with
interleukin-12 (IL-12) to address his
progressive KS 3 weeks later. IL-12 is
a glycoprotein cytokine that augments
type 1 immunity by promoting the de-
velopment of Th-1-type helper T cells
and also boosts natural killer cell lytic
activity. 30 The patient demonstrated
a partial remission of his KS at week
24 and a concomitant resolution of his
lower extremity pain during kneeling.
9ED9BKI?ED
T
his resident’s case problem
has highlighted the important
role of a thorough history, systems
review, and examination in the multi-
disciplinary management of a patient
with HIV, AIDS-related KS, and knee
pain. The clinical course of our patient
illustrated the clinical challenges posed
by systemic disease that can yield symp-
toms similar to common orthopaedic
conditions. The differential diagnosis
was further complicated by the incon-
gruent relationship of radiographic
signs of knee OA with knee pain and
disability, 37 and the myriad signs and
symptoms associated with PFPS.45
AIDS-related KS is more than a malig-
nancy that affects the integumentary
system. While it typically has a benign
cutaneous clinical presentation, this
neoplasm may spread to musculoskel-
etal tissues and result in focal pain and
functional limitations.14,20 The develop-
ment of increasingly effective antiretro-
viral agents has transformed HIV into a
chronic progressive disease. Therefore,
physical therapists who manage or-
thopaedic conditions in hospitals and
outpatient clinics should be aware of
the disablement that may result from
AIDS-related KS. T
616 | august 2009 | volume 39 | number 8 | journal of orthopaedic & sports physical therapy
ACKNOWLEDGEMENTS: The authors would like
to thank Dr Richard F. Little, Dr Ellen Miller,
Dr Galen Joe, Dr Julie Hobbs, CDR Michaele
Smith, Dr Danah Jack, and Dr Charles Mc-
Garvey for reviewing all or portions of the
manuscript.
H;<;H;D9;I
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journal of orthopaedic & sports physical therapy | volume 39 | number 8 | august 2009 | 617