118

Osteochondroses
Franklin Danger, MD1 Christopher Wasyliw, MD2 Laura Varich, MD3

1 Department of Radiology, Florida Hospital, Orlando, Florida
2 Division of Musculoskeletal Imaging, Department of Radiology,
Florida Hospital, Orlando, Florida
3 Division of Pediatric Imaging, Department of Radiology, Florida
Hospital, Orlando, Florida
Address for correspondence Laura Varich, MD, Division of Pediatric
Imaging, Department of Radiology, Florida Hospital, 601 E. Rollins
Street, Orlando, FL 32803 (e-mail: Laura.Varich.MD@flhosp.org).

Semin Musculoskelet Radiol 2018;22:118–124.

Abstract The osteochondroses are a group of disorders that affect the epiphysis or epiphyseal
equivalent segments of the immature skeleton. These disorders are believed to be
primarily the result of traumatic or vascular pathology, often in the setting of overuse,
Keywords and are usually self-limited. Their imaging findings are based on the time of the study
► osteochondrosis within the natural course of the disease process. Early findings may best be demon-

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► osteonecrosis strated by magnetic resonance imaging or may be recognized radiographically as
► avascular necrosis sclerosis of the involved segment. Later disease demonstrates bone fragmentation and
► child collapse, followed by healing where bone architecture is restored with variable
► adolescent reconstitution of the normal morphology.

The disorders classified as osteochondroses may at first seem
a heterogeneous group of loosely related disorders, but the
conditions have much commonality. Osteochondroses affect
the immature skeleton, follow similar natural courses, have
similar imaging findings, are most often treated conserva-
tively, and end with self-limited disease progression that
halts at skeletal maturity. Differences in the disorders are
based on affected sites and potential etiologic factors.
Differing terminology and classification within the litera-
ture continue to confuse the discussion of osteochondroses.
The terms “osteochondrosis,” “osteochondritis,” and “apo-
physitis” are often used interchangeably, and this lack of
semantic uniformity can be problematic. In addition, there is
inconsistent inclusion of various osteonecrotic entities with
heterogeneity in age of onset, clinical progression, and
prognoses. This article uses only the term “osteochondroses”
in discussing the conditions that meet the general criteria
presented in the previous paragraph and does not include
progressive osteonecrosis that occurs in adulthood (such as
Kienböck’s disease) or lesions of osteochondritis desiccans
(OCD). Differentiation between the osteochondroses and
OCD is critical because the osteochondroses appear at a
younger age, involve the entirety of the epiphysis or apo-
physis, and are self-limited, rarely requiring surgical treat-
ment. In contrast, OCD lesions present at an older age, involve
a small segment of the chondro-osseous junction at the
articular surface of the epiphysis, and more commonly result
in significant or long-term sequelae.
The osteochondroses affect epiphyses or epiphyseal
equivalents (apophyses, carpal, and tarsal bones) in specific
locations. Individual sites of osteochondroses were described
in the early 1900s, soon after Roentgen’s discovery of radio-
graph technology,1 and each is named after its discoverer(s).
The lesions that involve apophyses are believed to be trau-
matic in origin, related to asymmetric growth of the osseous
and myotendinous structures resulting in traction injury,2
and pathologic microtears and other evidence of trauma
have been identified.2 The etiology of the epiphyseal lesions
is more highly debated, with one or multiple contributing
factors including endocrine, genetic, traumatic, and vascular
causes as well as rapid growth.3
Patients with osteochondroses present in childhood or
adolescence with pain and disability.4 In general, the osteo-
chondroses affect boys more frequently than girls, likely due
to increased exposure to trauma and overuse injuries.4
The imaging findings identified in patients with osteochon-
droses vary depending on the stage of pathology at the time of
imaging. The initial pathologic stage involves necrosis of bone
and cartilage, followed by revascularization and granulation
tissue formation. Next, osteoclast resorption of necrotic tissue

Issue Theme Pediatric Musculoskeletal Copyright © 2018 by Thieme Medical DOI https://doi.org/
Imaging; Guest Editors, Ramesh S. Iyer, Publishers, Inc., 333 Seventh Avenue, 10.1055/s-0038-1627094.
MD and Matthew Cody O’Dell, MD, MPH New York, NY 10001, USA. ISSN 1089-7860.
Tel: +1(212) 584-4662.

and subsequent osteoid replacement with formation of
mature lamellar bone occurs.3 Much of our understanding of
the pathologic process of osteochondroses comes from the
study of Legg-Calvé-Perthes disease (LCP). As the osteochon-
drosis most frequently imaged, LCP has been extensively
characterized in the radiologic literature, allowing this specific
condition to serve as a guide to the imaging stages of osteo-
chondroses in general. Evolution of the disease process is most
often evaluated by radiographs or magnetic resonance ima-
ging (MRI). In the early stages of the osteonecrosis, radiographs
may demonstrate abnormal sclerosis; however, radiographs
may also appear normal, in which case the pathology may be
better detected by MRI. The weakened necrotic bone, if sub-
jected to stress, will then undergo fragmentation and collapse.
Later disease stages will demonstrate evidence of healing with
revascularization noted on MRI,5 followed by remodeling of
bone architecture, variable reconstitution of the normal mor-
phology, and return to normal MR signal intensity.5
In many patients with osteochondroses, symptoms resolve
spontaneously, with disease progression ceasing at the time of
skeletal maturity. When treatment is recommended, it is
routinely conservative including rest, unloading of pressure,
anti-inflammatory medications, and stretching. Rarely, conser-
vative treatment fails, and surgical treatment may be required.
The remainder of this article describes each specific
osteochondrosis by location, with discussion of its unique
clinical findings, imaging features, treatment, and prognosis.
Panner Disease
Panner disease is the most common cause of lateral elbow pain
in children < 10 years of age6 and is an osteochondrosis of the
humeral capitellum. This male-predominant disorder presents
between 5 and 10 years of age and is usually not associated with
repetitive trauma.7 Panner disease is self-limited, with regen-
eration of the capitellum in 12 to 18 months.2 In this context,
differentiation from capitellar OCD is important. In OCD, find-
ings occur in older patients (11–17 years) and are related to
Fig. 1 A 7-year-old male basketball player with Panner disease. (a) Frontal radiograph of the elbow demonstrates fragmentation and sclerosis of
the capitellum (arrow). (b) Coronal T1-weighted and (c) T2-weighted MRI images demonstrate bone marrow edema (low signal intensity on T1
and high signal intensity on T2) (arrowheads) intermixed with areas of sclerosis (very low signal intensity on both sequences) within the
capitellum (arrows). (Images courtesy of Dr. Cody O’Dell.)
Osteochondroses Danger et al. 119
repetitive trauma with imaging abnormality noted anterolat-
erally at the articular surface. In OCD, the disease is progressive
with findings of sclerosis, focal lucency, flattening, and intra-
articular bodies.7 Additionally, surgery is a common treatment
for OCD, in contradistinction to Panner disease.
Symptoms of Panner disease are usually mild, with lateral
pain and limited extension of the elbow the most common
complaints.2 In Panner disease patients, the entire ossifica-
tion center may show evidence of fissuring, lucency, frag-
mentation, and change in countour4,7 by radiography
(►Fig. 1a). MR imaging often demonstrates heterogeneous
signal intensity related to a combination of sclerosis and
edema (►Figs. 1b, c). Panner disease is a self-limited process,
and complete healing usually results following rest and
conservative management.
Scheuermann Disease
In Scheuermann disease, osteonecrosis of the thoracic spine
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causes thoracolumbar kyphosis in patients 12 to 15 years of
age.8 A family history of Scheuermann disease is common, and
the disorder is believed to demonstrate an autosomal dominant
inheritance that results in the development of poor bone
matrix,9 with a smaller etiologic contribution from mechanical
loading.8 Scheuermann disease affects 5% of the population,8
and although often thought to have a male predilection, the sex
distribution is actually close to equivalent.9
The most common complaint at presentation is back defor-
mity,10 with occasional pain centered at the curve apex.8
Physical examination demonstrates deformity and a rigid
humpback that does not correct with extension.4 The most
important radiologic findings for the diagnosis of Scheuermann
disease are thoracic kyphosis measuring > 45 degrees and at
least one vertebral body wedging > 5 degrees11 (►Fig. 2). Other
commonly associated imaging features include end-plate irre-
gularity with Schmorl’s nodes and narrowed intervertebral disk
spaces.8 Less commonly, limbus vertebrae, scoliosis, and spon-
dylolisthesis may be seen.8,9
Seminars in Musculoskeletal Radiology Vol. 22 No. 1/2018
120 Osteochondroses Danger et al.
Fig. 2 Computed tomography scan in a 14-year-old boy with
progressive back pain due to Scheuermann disease demonstrates
increased thoracic kyphosis (lines measuring Cobb angle of
76 degrees), anterior wedging of multiple vertebral bodies, and
multiple Schmorl’s nodes (arrowheads) as well as degenerative
changes with diffuse disk space narrowing, sclerosis, and osteophytes
(arrows).
The long-term prognosis of Scheuermann disease is
unknown, although patients are believed to demonstrate a
higher incidence of long-term back pain than the unaffected
population.12,13 If the kyphosis is < 50 degrees, manage-
ment is conservative. For patients with pain or kyphosis
between 50 and 65 degrees, a brace is often considered,9 and
partial reversal of vertebral wedging has been noted follow-
ing bracing that continues until skeletal maturity is reached.8
Surgical correction and fixation is only considered in patients
who have a progressive kyphotic curvature > 70 degrees,
refractory pain, or neurologic deficit following attempted
conservative treatment.8,9 In such cases, surgical interven-
tion may result in diminished long-term back pain.14
Legg-Calvé-Perthes Disease
LCP is a relatively common pediatric hip disorder, primarily
affecting children between 4 and 8 years of age, and with boys
affected 4 to 5 times more frequently than girls.1,4,15 Unilateral
LCP is more common, and if bilateral disease is noted, seen in
10 to 15% of patients, it is almost always asynchronous.16
Indeed, if bilateral and symmetrical disease is seen, other
etiologies of osteonecrosis should be considered.1
The condition results from the interruption of blood flow
to the hip.17 A vascular insult, currently of unknown etiology,
combined with repetitive loading leads to osteonecrosis of a
variable portion of the epiphysis,1 followed by resorption of
necrotic bone, trabecular collapse, and epiphyseal fragmen-
Seminars in Musculoskeletal Radiology Vol. 22 No. 1/2018
tation. Complete healing occurs over 2 to 4 years as woven
bone is laid down, followed by mature lamellar bone.17 Of
note, the initial ischemia and later neovascularization during
repair can affect the adjacent physeal cartilage and lead to
growth disturbances.16
The main clinical findings of LCP are limp, pain (within the
groin, hip, or knee), and limited joint motion.4,17 The goals of
imaging are to confirm the diagnosis, evaluate the extent of
local skeletal involvement, identify any contralateral disease,
and note any evidence of deformity.16 The earliest radiographic
finding is sclerosis of the affected femoral head. A widened
medial joint space, small ossific nucleus, and osteopenia of the
acetabulum and metaphysis may be noted.1,16 As the disease
progresses, a subchondral lucency and collapse may be seen
affecting the anterior femoral head, most conspicuous radio-
graphically on frog-leg lateral radiograph16 (►Fig. 3a). The
sclerosis eventually resolves as the bone architecture is
restored, and after healing, chronic deformity may be seen
related to growth plate and epiphyseal damage, resulting in a
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broadened femoral head and neck (coxa magna), flattened
femoral head (coxa plana), shortened femoral neck (coxa
breva), and joint incongruity (►Fig. 3c).18,19
At the earliest stages of LCP, MRI may be useful for doc-
umenting the presence of disease where a decrease in the lipid
content of the ischemic bone5 results in decreased T1 signal
intensity and increased T2 signal intensity.19 Dynamic con-
trast-enhanced perfusion imaging was shown to have
improved sensitivity over noncontrast-enhanced MRI for diag-
nosing avascular necrosis20,21 (AVN) where necrotic regions
show decreased peak enhancement. To avoid false-negative
results, it was suggested that MRI imaging performed in the
early stages of AVN (within the first 8 months of symptoms)
should include contrast enhancement.5
In later stages of LCP, MRI is beneficial in evaluating the
extent of involvement, the degree and location of collapse,
the presence of contralateral disease, evidence of healing,
the degree of physeal involvement, and residual defor-
mity.16,22 Decreased signal intensity will be noted in the
region of necrosis (►Fig. 3b). A characteristic appearance is
decreased signal intensity, the “double line” or “crescent”
seen within the anterior femoral head on T1- and T2-
weighted imaging, correlating with the presence of a sub-
chondral fracture.19,23
Presentation in children < 4 years of age is often asso-
ciated with a more favorable prognosis; a poorer prognosis is
associated with presentation at > 6 years of age, femoral
head deformity, joint incongruity, and decreased range of
motion.19,24,25 The percentage of femoral head involvement
and degree of epiphyseal extrusion are also important prog-
nostic factors.17 Early diagnosis and treatment is critical to
prevent secondary degenerative disease of the hip and avoid
femoral head deformation. The focus of therapy is the con-
tainment of the femoral head within the confines of the
acetabulum17 to protect the femoral head from deformation.
Containment can be achieved in younger children (< 5 years
of age) with milder disease by bracing and in older patients
or those with more severe disease through surgical osteot-
omy of either the femoral neck or acetabulum.17
 Osteochondroses Danger et al. 121

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Fig. 3 Legg-Calvé-Perthes (LCP) disease in a 5-year-old girl presenting with left hip pain. (a) Frog-leg lateral radiograph demonstrates flattening
of the femoral head and a subchondral lucency (crescent sign) (arrowheads). (b) T2-weighted MRI demonstrates femoral head collapse,
decreased signal intensity in the area of necrosis (large arrow), joint effusion (arrowheads), and increased T2 signal intensity within the
remainder of the femoral head and within the metaphysis (small arrows), suggestive of edema. (c) Anteroposterior pelvis radiograph in the same
patient four years after her initial diagnosis demonstrates chronic sequelae of LCP with femoral head flattening (coxa plana) (arrowheads),
broadened femoral head (coxa magna) (arrows), and shortened femoral neck (coxa breva).

Sinding-Larsen-Johansson and Osgood-
Schlatter Diseases
Sinding-Larsen-Johansson (SLJ) and Osgood-Schlatter (OS)
diseases are grouped together here because both represent
overuse injuries that affect the incompletely ossified struc-
tures at both the origin and the insertion of the patellar
tendon. Both processes affect boys more commonly with OS
disease predominantly presenting between 10 and 15 years
of age; SLJ presents at 9 to13 years.26
Traction on the patellar tendon results in microtears at the
insertions on the inferior patella and tibial tubercle causing
small avulsions of the cartilaginous attachments.27 The avulsed
cartilage fragments may ossify, and heterotopic ossification
may develop in the region of microtears.27 Patients with both
conditions present with anterior knee pain worsened by run-
ning or jumping.26 Point tenderness may be elicited over the
inferior pole of the patella (SLJ) or tibial tubercle (OS).
Radiographic findings include a fragmented appearance
of the tibial tubercle (OS) or inferior pole of the patella (SLJ),
with thickening of the proximal (SLJ) or distal (OS) patellar
tendon and edema of the fat superficial and deep to the
patellar tendon (►Fig. 4a, c). MRI may reveal thickening and
edema of the patellar tendon, infrapatellar bursitis, and
anterior soft tissue swelling26 (►Fig. 4b, d). Prognosis for
both OS and SLJ patients is excellent because both conditions
are self-limited. Conservative management is standard,
involving a combination of rest, ice, analgesics, and flexibility
exercises. In the rare patient in whom intratendinous bone
fragments persist adjacent to the tibial tubercle after skeletal
maturity (►Fig. 4e), surgical excision of the ossicles may be
required.2
Kohler Disease
Kohler disease affects the tarsal navicular, is more common
in boys, and usually is diagnosed between 2 and 8 years of
age.4 Kohler disease is unilateral in 75% of cases.3 Of note,
similar findings of sclerosis and collapse can be seen in
asymptomatic individuals, and thus the disease process
may be radiographically indistinguishable from the normal
variant appearance.

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122 Osteochondroses Danger et al.

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Fig. 4 (a, b) A 9-year-old male soccer player with Sinding-Larsen-Johansson disease. (a) Lateral radiograph of the knee demonstrates thickening
of the proximal patellar tendon (arrowheads), and fragmentation of the inferior pole of the patella (arrow). (b) Sagittal T2-weighted MRI shows
edema of the inferior pole of the patella (long arrow), proximal patellar tendon (arrowheads), and Hoffa’s fat pad (short arrows). (c, d) A 13-year-
old basketball player with Osgood-Schlatter (OS) disease. (c) Lateral radiograph demonstrates distal patellar tendon thickening (arrowheads)
and fragmentation of the tibial tubercle (arrow). (d) Sagittal MRI shows thickening and edema of the inferior patellar tendon (arrowheads) and
mild edema of the tibial tubercle (arrow). (e) Lateral radiograph in a 15-year-old boy demonstrates chronic change of OS with multiple ossicles
within the patellar tendon (arrows).

The symptoms of Kohler disease are typically mild, with

pain and point tenderness in the medial aspect of the mid-
foot. The resulting limp characteristically involves increased
weight-bearing on the lateral side of the affected foot.3
Because Kohler disease shares imaging characteristics
with normal variant ossification of the navicular, clinical
symptomology must be present to make a diagnosis. The
classic imaging findings include increased density, fragmen-
tation, and flattening of the navicular (►Fig. 5). Soft tissue
edema may also be appreciated.
The prognosis of Kohler disease is typically excellent,28
with complete restoration of the navicular occurring within a
few months.2 Treatment is thus focused on symptom relief
and is achieved through rest, plantar orthotics, and occa-
sional cast immobilization.2

Sever Disease
Sever disease involves the calcaneal apophysis and results
from repeated Achilles tendon traction2 or from compression
from axial loading.29 Typically bilateral and asymmetric,2
Fig. 5 A 6-year-old male soccer player with Kohler disease. Lateral
radiograph of the foot demonstrates sclerosis and flattening of the
tarsal navicular (arrow).

Seminars in Musculoskeletal Radiology Vol. 22 No. 1/2018

 Osteochondroses Danger et al. 123

Fig. 6 A 12-year-old female gymnast with Sever disease. (a) Lateral radiograph demonstrates sclerosis of the calcaneal apophysis (arrowheads).
(b) Sagittal MRI in the same patient demonstrates increased T2 signal intensity within the apophysis (arrowheads) and fluid signal intensity
within the physis (arrow) consistent with edema.

Sever disease affects adolescents 12 to 15 years of age. High may be helpful in demonstrating edema of the calcaneal

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levels of activity and obesity are both risk factors.29
The most common symptom of Sever disease is posterior
heel pain aggravated by rigorous physical activity. Tender-
ness over the insertion of the Achilles tendon can be elicited.
The patient may display a limp that avoids heel contact
during gait29 and interferes with physical activities.
Although there has been debate on the need for radiographic
evaluation in clinically suspected Sever disease,30 imaging
seems particularly important to exclude a more serious source
of symptoms, such as calcaneal stress fracture.2,31 Radiography
may show fragmentation and sclerosis of the calcaneal apo-
physis (►Fig. 6a), but because this finding can be seen in
asymptomatic patients, clinical correlation is imperative. MRI
apophysis in affected patients3 (►Fig. 6b), where its more
focal nature should allow differentiation from the increased T2
signal of normal hematopoietic marrow in children.
Prognosis for Sever disease patients is excellent, with pain
typically subsiding within 2 weeks to 2 months of onset if
treated appropriately with restricted weight-bearing, ice,
and analgesics.3 If symptoms are severe, a cast may be placed
for immobilization.
Freiberg Disease
Freiberg disease, also known as Freiberg infraction, is usually
diagnosed in adolescents between 12 and 18 years of age, with

Fig. 7 A 15-year-old female runner with Freiberg disease. (a) Oblique radiograph demonstrates flattening and irregularity of the second
metatarsal (MT) head (arrowhead). (b) Computed tomography scan in the same patient obtained 2 years later shows further flattening and
fragmentation of the MT head (arrows).

Seminars in Musculoskeletal Radiology Vol. 22 No. 1/2018

124 Osteochondroses Danger et al.
a significant female predominance. The etiology is likely
multifactorial, with trauma, vascular insufficiency, genetic
predisposition, and altered biomechanics as proposed causes
of the disease.32 Freiberg disease affects the second and third
metatarsal heads most commonly; involvement of the fourth
and fifth metatarsals is rare.32 The disease process is classically
unilateral, but bilateral disease is identified in up to 10% of
cases.4
Clinical findings in Freiberg disease include localized
pain worsened by weight-bearing, point tenderness, and
swelling.4
Early findings may include widening of the metatarsopha-
langeal joint. However, such findings may be absent on plain
radiography, and MRI may therefore be more sensitive for
diagnosis early on, demonstrating hypointensity of marrow
on T1-weighted images, and either low or high signal intensity
on T2-weighted or short tau inversion recovery sequences.28
Surrounding soft tissue edema may also be demonstrated by
MRI. Later in the pathologic process, cortical irregularity, frag-
mentation, and flattening of the metatarsal head may be seen by
radiography, computed tomography, or MRI28,33(►Fig. 7).
Standard treatment in Freiberg disease includes rest and
unloading of the affected metatarsal.3,32 Early treatment
results in complete healing,32 with improvement of metatarsal
head morphology on radiographs evident at 2 to 3 years.3
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