Musculoskeletal Imaging, The Essentials - Chew (2019)

Musculoskeletal
Imaging
THE
ESSENTIALS
Felix S. Chew, MD
Professor
Section Chief, Musculoskeletal Radiology
University of Washington
Seattle, Washington
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Copyright © 2019 Felix S. Chew.
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Library of Congress Cataloging-in-Publication Data
Names: Chew, Felix S., editor.

Title: Musculoskeletal imaging : the essentials / [edited by] Felix S. Chew.
Other titles: Musculoskeletal imaging (Chew) | Essentials (Philadelphia, Pa.)
Description: Philadelphia : Wolters Kluwer, [2019] | Series: Essentials series |
Includes bibliographical references and index.
Identifiers: LCCN 2018020189 | ISBN 9781496383860
Subjects: | MESH: Musculoskeletal diseases—diagnostic imaging | Fractures,
Bone—diagnostic imaging
Classification: LCC RC925.7 | NLM WE 141 | DDC 616.7/075—dc23 LC
record available at https://lccn.loc.gov/2018020189
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CONTRIBUTORS
Sandra J. Allison, MD
Associate Professor
Department of Radiology
Georgetown University School of Medicine
Washington, DC
Stanislav Belchuk, MD
Resident
Department of Diagnostic and Interventional Imaging
McGovern Medical School
The University of Texas Health Science Center at Houston
Houston, TX
Luis S. Beltran, MD
Associate Professor
New York University School of Medicine
New York, NY
Blake Carlson, MD
Acting Instructor & Senior Fellow
University of Washington Medical Center
Seattle, WA
Felix S. Chew, MD
Professor
Seattle, WA
Jennifer L. Favinger, MD
Clinical Instructor
Seattle, WA
Kimia Khalatbari Kani, MD

Assistant Professor
University of Maryland
Baltimore, MD
Manickam Kumaravel, MD
Associate Professor
Diagnostic and Interventional Imaging & Orthopedics
University of Texas Health Science Center at Houston
Houston, TX
Hyojeong Mulcahy, MD
Associate Professor
Seattle, WA
Erika M. Nealey, MD
Radiologist
St. Elizabeth Hospital
Enumclaw, WA
Refky Nicola, DO
Radiologist
SUNY Upstate Medical University
Syracuse, NY
Jack Porrino, MD
Associate Professor
Department of Radiology & Biomedical Imaging
Yale School of Medicine
New Haven, CT
Michael L. Richardson, MD
Professor
Seattle, WA
Stacy E. Smith, MD
Associate Professor
Harvard Medical School
Boston, MA
Ryan Tai, MD
Assistant Professor
University of Massachusetts Medical School
Worcester, MA
Sean Wo, MD
Resident
Seattle, WA
SERIES FOREWORD
he Essentials series is a collection of radiology textbooks following a

T standardized format. Each book in The Essentials series is a practical tool
for those wanting to quickly acquire a broad base of knowledge in a
specialty area. The content is limited to the essentials of that specialty so as not
to overwhelm the novice yet provides enough detail that it can serve as a quick
review for residents or practicing radiologists, a guide for those who teach the
specialty, and a reference for specialty physicians and other health care
professionals whose patients are referred for imaging in that specialty area. What
sets The Essentials texts apart from other similar texts is that they (1) are
compact and of practical size for a resident to read during an initial 4-week
rotational experience, (2) include learning objectives at the beginning of each
chapter, and (3) provide an exercise for self-assessment. Each book includes
citations from the most recent literature that are called out in the text.
Self-assessment is a key component of The Essentials texts. Multiple-choice
items are included at the end of every chapter, and a self-assessment examination
is included at the end of each text. This should be of particular benefit to those
who are preparing for the new image-rich computer-based examinations that are
a component of professional certification and maintenance of certification.
The series not only includes texts related to clinical specialties that are rich
with radiologic images and illustrations but also texts related to noninterpretive
subjects such as radiologic physics and quality and safety in medical imaging.
The goal of The Essentials series is to provide a collection of practical references
to accompany a well-rounded education in diagnostic imaging and imaging-
guided therapy.
JANNETTE COLLINS, MD, MED, FCCP, FACR

P R E FA C E
his book was written with 2 primary objectives: (1) to provide the
T essential knowledge that residents need to be successful in their first 3
years of diagnostic radiology training and (2) to help prepare residents for
the core portion of the certification examination. When coupled with the
appropriate duration of supervised practical clinical experience and a series of
regular teaching conferences, the reader should be more than adequately
prepared to pass the musculoskeletal imaging section of the examination. This
book supports the musculoskeletal radiology curriculum for radiology residents
created by the Society for Skeletal Radiology.
Because musculoskeletal medicine is not well covered in most undergraduate
medical school curricula, underlying basic science and relevant clinical
principles are discussed and correlated with imaging throughout the book. The
first portion of the book covers the diagnosis of fractures and dislocations by
radiography and CT, followed by a chapter on the imaging of fracture treatment
and healing. Relevant biomechanical and anatomic principles are introduced and
used as a basis for discussion and deeper understanding. The next several
chapters address MRI of injuries in various anatomic regions, including practical
discussions on interpretation and relevant pathoanatomy. Imaging of bone
tumors and soft tissue masses is next, including benign, malignant, and
metastatic lesions. Analysis and diagnosis of these lesions relies heavily on
clinical, radiologic, and pathologic correlation and imaging with multiple
modalities. Chapters on arthritis and other joint conditions, including the chapter
dedicated to the foot, are followed by chapters on joint replacement and other
postsurgical imaging topics. The book closes with chapters on miscellaneous
topics including skeletal dysplasia in the adult, osteoporosis and disorders of
mineral metabolism, systemic conditions affecting the musculoskeletal system,
musculoskeletal infection, bone marrow disorders, musculoskeletal ultrasound,
and musculoskeletal interventional procedures. There are 4 self-assessment
questions at the end of each chapter and a final collection of 100 self-assessment
questions at the end of the book that covers the spectrum of musculoskeletal
imaging.
As this book is part of the Essentials Series of radiology textbooks, we have
chosen not to duplicate 2 subject areas that are included in other books in the
series. Spine imaging is found in Neuroimaging: The Essentials, by Sanelli,
Schaefer, and Loevner, and pediatric musculoskeletal imaging is found in
Pediatric Imaging: The Essentials, by Iyer and Chapman.
FELIX S. CHEW
CONTENTS
Contributors
Series Foreword
Preface

Chapter 1 Imaging Basics of Musculoskeletal Trauma

Felix S. Chew
Chapter 2 Imaging of Upper Extremity Fractures and Dislocations

Manickam Kumaravel, Refky Nicola, Stanislav Belchuk, and Felix S. Chew
Chapter 3 Imaging of Lower Extremity Fractures and Dislocations

Refky Nicola, Manickam Kumaravel, Stanislav Belchuk, and Felix S. Chew
Chapter 4 Imaging of Fracture Treatment and Healing

Felix S. Chew
Chapter 5 MRI of Knee Injuries

Felix S. Chew and Kimia Khalatbari Kani
Chapter 6 MRI of Shoulder Injuries

Luis S. Beltran
Chapter 7 MRI of Elbow Injuries

Hyojeong Mulcahy
Chapter 8 MRI of Hip Injuries

Stacy E. Smith, Ryan Tai, and Felix S. Chew
Chapter 9 MRI of Wrist and Hand Injuries

Hyojeong Mulcahy and Felix S. Chew
Chapter 10 MRI of Ankle and Foot Injuries

Chapter 11 Imaging Basics of Bone Tumors

Felix S. Chew
Chapter 12 Imaging of Benign Bone Lesions

Kimia Khalatbari Kani and Felix S. Chew
Chapter 13 Imaging of Malignant Bone Tumors

Felix S. Chew
Chapter 14 Imaging of Musculoskeletal Metastases

Felix S. Chew
Chapter 15 Imaging of Soft-Tissue Lesions and Calcifications

Felix S. Chew
Chapter 16 Imaging Basics of Arthritis

Michael L. Richardson
Chapter 17 Imaging of Osteoarthritis

Michael L. Richardson and Felix S. Chew
Chapter 18 Imaging of Inflammatory Arthritis

Chapter 19 Noninflammatory Joint Disease

Chapter 20 Imaging of Nontraumatic Foot Conditions

Felix S. Chew
Chapter 21 Imaging of the Postsurgical Lower Extremity

Chapter 22 Imaging of the Postsurgical Upper Extremity

Felix S. Chew
Chapter 23 Imaging of Bone Dysplasias in Adults
Chapter 24 Osteoporosis and Abnormal Mineral Metabolism

Chapter 25 Imaging of Systemic and Metabolic Musculoskeletal

Conditions
Chapter 26 Imaging of Musculoskeletal Infections

Jennifer L. Favinger and Felix S. Chew
Chapter 27 Imaging of Bone Marrow Conditions

Erika M. Nealey, Blake Carlson, and Felix S. Chew
Chapter 28 Musculoskeletal Ultrasound

Felix S. Chew and Sandra J. Allison
Chapter 29 Procedures in Musculoskeletal Radiology

Sean Wo and Jack Porrino
Self-Assessment Questions
Index
1
Imaging Basics of Musculoskeletal
Trauma
Felix S. Chew
Trauma is the reason most radiographs of the musculoskeletal system are

ordered. Radiography is a rapid, inexpensive, and widely available method for
detecting, characterizing, and following fractures.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging basics of musculoskeletal trauma,
the learner will be able to
1. discuss and recommend appropriate imaging strategies,
2. describe radiologic features, and
3. summarize relevant concepts and knowledge for the following topics: fracture epidemiology,
bone biomechanics, imaging of fractures, soft-tissue biomechanics, imaging of soft-tissue
injuries, open fractures, gunshot wounds, burns and blast injuries, stress injuries, fracture
description, and fracture classification.
FRACTURE EPIDEMIOLOGY
Below the age of 50 years, fractures are much more common in men than in
women, but above this age, fractures become more common in women. This
distribution is the result of greater exposure to trauma in men at younger ages
and the postmenopausal deterioration of the musculoskeletal system in older
women. Using data from Olmsted County, MN, Amin et al1 found that in the
population aged 50 years and older, women experienced 1.5 times as many
fractures as men. The most common cause was a fall from standing height; 33%
of the fractures resulted from severe trauma such as motor vehicle crashes or
falls from heights; only 2% of all fractures were pathologic. The overall
incidence of fractures for this population was almost 3% per year, but the
incidence increased with age. In young adults, the most common sites of
fractures in the extremities are hand, distal humerus, tibial shaft, clavicle, distal
radius, and foot. In women aged 50 years and above, the top sites for extremity
fractures are foot, distal radius, ankle, proximal femur, and hand. In men aged
50 years and above, the top sites for extremity fractures are hand, proximal
femur, foot, ankle, and clavicle.
BONE BIOMECHANICS
Bone responds to trauma in predictable ways.2 The anatomy and morphology of
fractures frequently suggest the forces that caused it. There are practical
applications of this knowledge to diagnosis and management.
Force and Deformation

Application of external force to bone is called loading. Bone is physically
deformed (ie, undergoes strain) when it is placed under a load (Figure 1.1). At
physiologic levels of loading, bone undergoes elastic deformation, as it absorbs
and stores the energy imparted by the loading. When the load is removed, the
stored energy is dissipated by elastic recoil, the bone recovers its preloaded
shape, and no damage is sustained. Loading has a linear relationship to elastic
deformation called stiffness. The stiffer the material, the less it deforms under a
given load. When the severity of loading exceeds the level at which elastic recoil
is possible, the bone sustains plastic (also called ductile) deformation. The
absorbed energy from loading is expended in the work of permanently
deforming the bone. The ductility of a material describes the degree to which it
can sustain plastic deformation without breaking. At even greater levels of
loading, the bone fails completely, and the imparted energy is expended in
fracturing the bone and displacing the fragments. If loading continues, other
body parts may sustain injury. Excessive loading results in injury; in general, the
greater the amount of loading and the more rapidly it is applied, the more severe
the injury.
The external force of loading involves 3 fundamental components:
compressive, tensile, and shear. The compressive component acts inwardly and
squashes the bone together; the tensile component acts outwardly and pulls the
bone apart; and the shear component acts parallel to the direction of force and
sends different points in the bone past each other. Bone subjected to tensile
loading tends to elongate; mechanical failure occurs when cement lines debond
and the osteons are pulled apart. Bone subjected to compressive loading tends to
shorten; mechanical failure occurs when individual osteons sustain oblique
cracking. Bone subjected to shear loading undergoes angular deformity. Both
tensile and compressive loading have shear as a component because angular
deformity occurs as bone elongates or shortens.
•
FIGURE 1.1 Various modes of loading.
Bone is a diphasic material composed of a rigid calcium hydroxyapatite

crystalline structure, which is resistant to compressive forces, and a collagenous
matrix of flexible fibrils and ground substance, which is resistant to tensile
forces. In compact bone (also referred to as lamellar bone or cortical bone), the
material of bone is organized into concentric layers around the neurovascular
supply to form osteons (haversian systems). Osteons are the basic functional and
structural unit of compact bone. In cancellous bone (trabecular bone), the
material of bone is organized into a 3-dimensional latticelike system of plates
and columns (trabeculae), with the neurovascular supply passing between
trabeculae. Compact bone is stiffer than cancellous bone, but cancellous bone is
more ductile. The functional architecture of mature bone reflects a continuing
process of remodeling to accommodate the type, magnitude, and direction of
physiologic loading. In general, bone resists compression better than tension and
tension better than shear.
Loading and Fractures

Loading can be direct or indirect. Direct loading causes injuries at the site of
loading. The morphology of fractures caused by direct loading—although related
to the site, direction, and amount of force applied—tends to be unpredictable.
Such injuries may be classified as crushing, penetrating, or tapping. A crushing
injury results from the application of a large force over a large area, for example,
a building collapsing on an individual. Crushing force results in comminuted or
transverse fractures and extensive soft-tissue damage. A penetrating injury
results from a large force being applied to a small area, for example, a gunshot
wound. Penetrating force usually results in comminuted fractures; the degree of
comminution depends on the energy of the penetrating projectile (Figure 1.2). A
tapping injury results from a small force being applied to a small area, for
example, a blow to the forearm from a nightstick. Tapping force results in a
transverse or stellate fracture at the site of impact (Figure 1.3). Bones without
much soft-tissue coverage, such as the ulna or tibia, are more vulnerable to direct
trauma than bones such as the humerus or femur.
•
FIGURE 1.2 Low-velocity gunshot wound causing comminuted fractures of the
ulnar shaft.
•
FIGURE 1.3 Tapping fracture of the ulnar shaft (nightstick fracture).
Indirect loading causes injuries at a distance from the site of loading. The
morphology of fractures caused by indirect loading tends to be predictable.
Loading under tension (pulling apart), compression (squashing together), torsion
(twisting), angulation (bending), and certain combinations of these produce
fractures with predictable shapes that often occur at specific sites (Figure 1.4).
The soft tissues may modify indirect loading—for example, muscles can reduce
tensile loads on bones by contracting and supplying an opposing compressive
force.
•
FIGURE 1.4 Types of loading correlated with direction of fracture lines.
•
FIGURE 1.5 Avulsion fragment at the extensor insertion at the distal phalanx
(arrow).
Traction or tension fractures result from traction on a bone by a tendon or

ligament. The bone is pulled apart, or avulsed, and the fracture line is transverse
to the direction of force, as the bone fibers fail under tension. At the fingers, for
example, fragments of bone may be avulsed at the insertions of tendons or
ligaments (Figure 1.5). The size of the avulsed fragment may range from large to
tiny (Figure 1.6). A large fragment may comprise a full-thickness piece of the
bone; a small fragment may represent a mere fraction of the cortex. Tension
fractures are most common in cancellous bone.
When a long bone is angulated, the convex side is placed under tension, and
the concave side is placed under compression. Because bone fails first under
tension, a transverse fracture propagates across the bone from the convex side.
On the concave side, the bone may fail under compressive and shearing forces
and splinter. Alternatively, a triangular fragment may shear off at an angle to the
main fracture line. This results in comminution with a butterfly fragment on the
concave side of the bend (Figure 1.7).
•
FIGURE 1.6 Tiny avulsion fragment at the volar plate attachment at the middle
phalanx (arrow).
•
FIGURE 1.7 Transverse fracture of the tibia with butterfly fragment.
Longitudinal compressive loading of the shaft of a long bone results in an

oblique fracture caused by osteons being forced past each other and shearing off
(Figure 1.8). Compressive loading of a whole bone often results in T- or Y-
shaped fractures, as the cortical bone of the shaft is driven into the cancellous
metaphysis. Such fractures are common at the ends of the humerus and femur.
Rotational loading (torsion or twisting) causes horizontal shearing with
compressive and tensile components at an angle to the long axis of the shaft
(Figure 1.9). These stresses lead to a spiral fracture that curves around the
circumference of the bone, representing a failure in tension, as the bone is pulled
apart. The fracture line makes 1 complete rotation around the circumference of
the bone and has sharp pointed ends joined by a vertical component (Figure
1.10). The vertical fracture acts as a hinge, with the fracture fragments
separating on the opposite side along the curved component.
•
FIGURE 1.8 Oblique fracture of the proximal phalanx of the middle finger.
Many fractures are produced by a combination of forces. Angulation with

axial compression results in a curved fracture line with oblique and transverse
components and sometimes a butterfly fragment. Angulation with rotation
results in an oblique fracture with short, blunted ends.
Bone Bruises
Bone bruises are traumatic injuries to cancellous bone in which hemorrhage and
edema displace the normal marrow.3 These injuries, which involve
microfractures of individual trabeculae and disruption of small vessels, are
evident on MRI as regions of localized edema with intact overlying articular
cartilage and subcortical bone. The mechanism of injury is typically
compression, either from direct loading or from indirect loading, with the
loading transmitted through an adjacent bone. When the mechanism is direct
loading, the bone bruise is usually isolated. When the mechanism is indirect,
transmitted loading, additional significant injuries may be present elsewhere in
the anatomic region (Figure 1.11). The pattern of bone bruises may help to
identify associated injuries and suggest the mechanism of injury. Bone bruises
typically revert to normal on follow-up MRI within several months; radiographs
may remain normal throughout the episode.
IMAGING FRACTURES
Although some fractures can be identified on virtually any imaging modality,
radiography dominates the imaging evaluation for acute fractures. CT has a
supporting role in characterizing complex fractures in preparation for possible
surgery and occasionally in identifying fractures when radiographs are
equivocal. In the spine, CT is used to screen for fractures in the setting of
polytrauma. MRI may be used for identifying fractures when radiographs or CT
are abnormal or equivocal and particularly for stress and insufficiency fractures.
MRI is more commonly used for identifying and characterizing soft-tissue and
joint injuries. The Tc-99m radionuclide bone scan may be used for identifying
stress fractures.
•
FIGURE 1.9 Diagrammatic representation of spiral fracture. On the near cortex of
the bone, under torsion, horizontal shear stress forces points in the bone past each
other. Tensile stress is present because these points are at the same time pulled
apart, leading to an obliquely oriented tension fracture around the circumference of
the bone. On the far cortex of the bone, compressive forces are present, leading to a
vertical fracture that joins the spiral fracture lines.
On radiographs, fractures of cortical bone are definitively recognized as focal

discontinuities in the structure of bone, particularly when displacement is
present. Impacted fractures of cortical bone may be recognized as focal
alterations in the contour of the bone, typically an abrupt change in what should
otherwise be a smooth contour. Compression fractures in cancellous bone may
have a discontinuity in cortex, a change in shape, a linear region of sclerosis, or
any combination of these features. Avulsion fractures occur when tension on the
attachment of a tendon, ligament, or capsule pulls off a fragment of bone. These
fractures may be recognized as a displaced fragment that may range in size from
less than 1 mm in thickness to several centimeters.
On CT scans, the features of fractures are similar to those seen on
radiography, but the ability to display the features is greatly enhanced by axial
cross sections, multiplanar reformations, and 3-dimensional reconstructions
(Figure 1.12).
On MRI, fracture lines are dark on T1, with surrounding intermediate signal
that may involve the adjacent marrow and soft tissues, corresponding to
hemorrhage and edema (Figure 1.13). On T2, the surrounding edema and
hemorrhage generally have high signal, while the fracture line remains dark. In
compression fractures of cancellous bone, the fracture line may be absent, but
the change in signal will be present if the fracture is acute. Avulsion fracture
fragments may be difficult to identify on MRI, as the fragment itself may have
the same dark signal on T1 and T2 as the soft-tissue structure that pulled it off.
Surrounding edema and hemorrhage should be present with acute fractures.
Fractures caused by compressive loading tend to have greater amounts of
adjacent marrow edema than fractures caused by tensile loading.
•
FIGURE 1.10 Spiral fracture of the tibial shaft. A, Anteroposterior radiograph. B,
Lateral radiograph.
•
FIGURE 1.11 Bone bruises caused by hyperextension injury. Sagittal T2 FS MRI
shows a bone bruise in the anterior aspect of the lateral tibial plateau and a matching
impaction fracture of the lateral femoral condyle.
On radionuclide bone scans, fractures are evident as regions of focal

accumulation of radioactivity. However, because a scan typically takes a couple
of hours to perform, radionuclide bone scans are not used in imaging acute
trauma.
SOFT-TISSUE BIOMECHANICS
The soft-tissue structures of the musculoskeletal system deform when loaded.2 In
addition to recoverable or elastic deformation, the soft tissues may also sustain
nonrecoverable or nonelastic deformation. Creep is continuous deformation
under an applied load, and stress relaxation is the decrease in an internal load
over time at a constant deformation. These viscous effects vary with time and the
rate of loading, and the structure does not instantaneously recover its original
size and shape when the load is removed. When a soft-tissue structure is loaded
rapidly, it deforms elastically and perhaps fails if the load is great enough; if the
same load is applied more slowly, creep and stress relaxation allow the structure
to deform further, permitting it to absorb more energy without failing. For these
reasons, ligaments and tendons are stronger under tensile loading when the load
is applied slowly than rapidly. Where they attach to bone, it is generally the rate
of loading and the strength of the soft tissues relative to the bone that determine
whether a soft tissue or a bony injury is sustained. In general, rapid rates of
loading cause the soft tissues to fail, whereas slower rates of loading avulse the
bone. Injuries of tendons or muscle-tendon units are called strains; injuries of
ligaments are called sprains. Injuries of either may also be called tears. Strains
and sprains are classified by severity, with grade 1 being a mild injury and grade
3 being a severe, complete discontinuity (Table 1.1). Injuries to soft tissue alone
without associated fractures are common and may be undetectable on
radiographs but may be directly imaged by MRI and sonography.
•
FIGURE 1.12 Subtle hip fracture on CT. A, Axial CT shows subtle discontinuity in
the right femoral cortex anteriorly with slight impaction posteriorly (arrows),
corresponding to a minimally displaced fracture of the greater trochanter. B, Coronal
CT shows extent of the fracture.
•
FIGURE 1.13 Minimally displaced lateral tibial plateau fracture. A, Coronal T1 MRI
shows dark fracture line (arrow) with surrounding edema. B, Coronal STIR MRI shows
dark fracture line (arrow) with surrounding edema.
Soft-tissue injury always accompanies bony injury. Damage may range from
superficial abrasions and minimal contusions at the site of injury to massive
devitalization involving major segments of the limbs. Direct trauma may cause
abrasion, contusion, or crushing of soft tissues. Subcutaneous avulsion of the
cutis, compartment syndrome, and major vascular injury may be caused by
indirect mechanisms. For example, displacing fragments from a fracture caused
by high-energy indirect loading may slice through the adjacent neurovascular
structures and surrounding soft tissues like a meat grinder. In the forearm and
lower leg, hemorrhage and acute inflammation from soft-tissue injuries may lead
to a compartment syndrome in which increased hydrostatic pressure within a
fascial compartment may compromise the circulation and cause ischemic
necrosis. Strains of adjacent musculature are common accompaniments to
fractures, and sharp bony fragments may lacerate adjacent muscles. Complete
fractures of long bones may result in hematomas and sterile collections when the
bone marrow spills into the adjacent soft tissues (Figure 1.14).
Table 1.1 GRADING OF SPRAINS AND STRAINS
Clinical Signs
Grade Injury Ligament Muscle-Tendon
1 Failure of a few fibers No laxity No weakness
2 Partial failure Laxity Weakness
3 Complete rupture Frank instability No muscle action
•
FIGURE 1.14 Hematoma and sterile collection of bone marrow spilling into the soft
tissues adjacent to a displaced femoral shaft fracture. Note the fat-fluid level
(arrowheads) on this horizontal beam radiograph, and the posterior displacement of
the calcified popliteal artery (arrow) by the collection.
The articular cartilage that covers the ends of bones in joints is usually loaded
in compression because the friction at the surface is too low to generate
significant shearing forces. With compressive loading, usually indirect blunt
impact transferred through the bone, the structure of the extracellular matrix may
sustain damage. With more severe loading, the chondrocytes may die, and the
cartilage may crack apart and become fissured. Fibrocartilage articular structures
such as articular discs, menisci, and labra may be injured by a variety of
mechanisms.
IMAGING SOFT-TISSUE INJURIES
Although radiography is typically the first imaging study used for evaluation of
soft-tissue injuries, it is performed principally to look for fractures. CT is
sometimes used in the same way, particularly in the spine. MRI is the best
imaging modality for identifying and characterizing soft-tissue and joint injuries.
The radionuclide bone scan is not useful in recognizing sprains and strains.
Sonography is typically not used by radiologists in the acute setting.
•
FIGURE 1.15 Ulnar collateral ligament sprain at the first metacarpophalangeal joint.
Fluoroscopic image with stress shows widening of the joint on the ulnar side (arrow).
On radiographs, injuries of ligaments and joint capsules (sprains) and of

muscle-tendon units (strains) may be recognized indirectly, evident as soft-tissue
swelling or the loss of anatomic positioning of bony structures. Stress views or
kinematic observation under fluoroscopy may be helpful (Figure 1.15). For
example, when bony structures stabilized by a ligament are displaced from their
usual positions, injury to the ligament may be inferred. Soft-tissue swelling,
particularly when focal, may also indicate a sprain or a strain.
On CT, the ability to identify soft-tissue structures is improved compared with
radiographs. As with radiography, indirect signs such as displacement of bony
structures or soft-tissue swelling may allow one to infer the presence of a sprain
or strain.
On MRI, sprains and strains may be directly imaged. Complete tears (grade 3
sprains) of ligaments may be evident as absence of the structure, displacement of
the structure, discontinuity of the structure, or abnormal signal intensity. When
tears are acute, displacement and discontinuity with surrounding hemorrhage and
edema allow a definitive diagnosis. Partial tears (grade 1 or 2 sprains) may be
evident as focally increased T2 signal with surrounding hemorrhage and edema;
at least some portions of the ligament remain in continuity. Complete tendon
tears (grade 3 strains) are usually evident as discontinuity of the tendon with
retraction in the direction of the muscle belly. Hemorrhage and edema are
typically present in the acute phase but may be absent if the injury is chronic.
When tears are partial (grade 1 or 2 strains), focally increased T2 signal is
present, sometimes with surrounding edema and hemorrhage. Abnormal
intrasubstance signal and swelling are generally present in all tendon tears. Fluid
within the tendon sheath is also a typical finding in both complete and partial
tendon tears. Muscle tears are evident as high T2 signal, corresponding to edema
and hemorrhage (Figure 1.16). The abnormal signal is distributed along fascial
planes and may be interdigitated within muscle fascicles.
•
FIGURE 1.16 Muscle strain accompanying fracture. Axial STIR MRI of the thigh
shows high signal in the vastus intermedius muscle (arrow) surrounding a femoral
shaft fracture.
On sonography, the appearance of normal ligaments, tendons, and muscles,

because they are structurally organized along lines of stress, is directionally
dependent, a property called anisotropy. Complete tendon tears may be
recognized by discontinuity of the tendon with the 2 ends separated by
hypoechoic blood, fluid, or granulation tissue.4 Sometimes, the structure is
simply absent from its expected location. Partial tears may be recognized as
focal hypoechoic defects within the substance of the tendon or focal thinning
(Figure 1.17). If a tendon sheath is present, fluid within the tendon sheath will be
interposed between the torn fragments of either complete or partial tears.
OPEN FRACTURES
Open fractures (also called compound fractures) involve a break in the skin.
These are distinguished from closed fractures (also called simple fractures), in
which the skin remains intact. The presence of a skin wound is often an
indication of extensive soft-tissue injury. Traumatized, devitalized soft tissues
pose a grave threat of infection; exposed bone will not heal. Radiographic signs
indicative of an open fracture include a soft-tissue defect, a bone fragment
protruding beyond the soft tissues, gas in the soft tissues or within an adjacent
joint, the presence of a foreign body, and missing bone fragments.
Open fractures can be classified by the energy of the injury and consequent
extent of soft-tissue devitalization.5,6 Type I open fractures are low-energy
wounds with a skin wound that is typically 1 cm or less in length. A sharp bone
fragment piercing the skin from the inside out usually causes the skin wound,
which is generally clean. Muscle and soft-tissue damage is minimal or absent.
These injuries are usually debrided and closed. The risk of infection under ideal
management is low. Type II open fractures are usually penetrating wounds with
fractures (Figure 1.18). The extent of soft-tissue injury is relatively localized, but
the skin wound is greater than 1 cm in length. These injuries may be debrided
and closed or left open, depending on circumstance. The infection rate is
approximately 2%. Type III open fractures are severe high-energy wounds with
gross disruption of skin, soft tissues, and bone. Extensive muscle devitalization
and soft-tissue disruption or gross contamination are present, and the skin wound
is often 10 cm or more in length. The associated fractures are widely displaced,
segmental, or badly comminuted, as one would expect with a high-energy injury
(Figure 1.19). Type III open fractures can be further classified into type III-A, in
which there is only limited stripping of the periosteum and soft tissues from the
bone; type III-B, in which there is extensive soft-tissue loss and gross exposure
of bone; and type III-C, in which there is a major vascular disruption. The
infection rate is approximately 18% for type III-A open fractures but is more
than 50% for types III-B and III-C open fractures. Paradoxically, as techniques
of surgical management have improved, the infection rate of open fractures has
increased. The explanation lies in the attempted salvage of more severely
traumatized limbs that previously would have simply been amputated. The
spectrum of infecting organisms has also been changing.
•
FIGURE 1.17 Sonogram of Achilles tear. A, Longitudinal scan (feet to left, head to
right) shows normal distal tendon fibers (arrowheads) and markedly thickened and
retracted proximal tendon (arrow) with heterogeneous echogenicity (Tibia = posterior
tibia). B, Sagittal PD MRI of the Achilles tendon with the sonographic field of view
indicated by the rectangle. The distal tendon has normal thickness (arrowheads),
whereas the retracted proximal tendon is thickened (arrow).
•
FIGURE 1.18 Amputation of a fingertip.
•
FIGURE 1.19 Comminuted open fracture of the foot from crush injury.
Open fractures that involve a joint often require special surgical care. Gas
within a joint that is adjacent to a fracture is an indication that the joint may be
contaminated and requires debridement and repair (Figure 1.20). If the joint was
dislocated as well as opened to the environment, contamination may be gross.
GUNSHOT WOUNDS
Bullets produce open wounds7; contaminated material such as clothing and skin
is carried deep into the wound. Because insufficient heat is generated during
firing and flight, bullets are not bacteriologically sterile. A bullet with a full
metal jacket does not fragment in tissue, but partially jacketed or unjacketed
bullets tend to expand, deform, and fragment, increasing the volume of the
injury. As established by convention, military small arms use fully jacketed
ammunition, but civilian small arms may use partially jacketed or unjacketed
ammunition. Many law enforcement agencies use unjacketed, hollow-point
bullets in their weapons to reduce the likelihood of a bullet passing through an
intended target and striking a bystander.
FIGURE 1.20 • Open, comminuted fracture-dislocation of the ankle. Lateral

radiograph shows fractures with air within the ankle joint (arrow). The joint had been
reduced at the scene of the injury before transport.
Low-velocity gunshot wounds are caused by pistols and many small-bore

civilian rifles (muzzle velocities of less than 1000 ft/s or 305 m/s). Tissues are
lacerated and crushed, as the bullet strikes and passes into the body. The entire
energy of the projectile often is absorbed at the site of impact, and the bullet
itself frequently comes to rest in the body. Low-velocity gunshot wounds that
involve bone are generally type II open fractures. The extent of soft-tissue injury
is restricted to the immediate path of the projectile. The path of the bullet in the
body may be erratic, following anatomic tissue planes and other paths of low
resistance, sometimes leaving trail of small metallic fragments. A bullet that
comes to rest in a body cavity or lumen may migrate or embolize. The size of a
bullet on radiographs depends on its actual size, the radiographic projection, and
the degree of magnification. CT may be helpful in localizing the bullet.
High-velocity gunshot wounds are caused by assault rifles and high-powered
hunting rifles (muzzle velocities of greater than 2000 ft/s or 610 m/s). Because
kinetic energy increases with the square of the velocity of a projectile, projectiles
from high-velocity weapons generally cause severe type III open wounds. On
impact, kinetic energy is rapidly transferred from the missile to the tissue. As a
high-velocity projectile passes through the body, it compresses the tissues along
its path, creating a transient shock wave. Shock waves can cause gas-filled
organs to rupture but cause little if any damage to muscle or bone. A temporary
vacuum cavity forms behind a high-velocity projectile, similar to turbulence that
forms behind a hand, as it is moved rapidly through water. The pressure within
the temporary cavity is subatmospheric, causing debris to be sucked into the
wound. The cavity oscillates violently and rapidly as it collapses, damaging an
extensive volume of tissue. If the projectile strikes bone, the bone shatters into
secondary projectiles. Vascular and neural structures may be extensively
damaged, and a volume of tissue extending around the path of the projectile for
several centimeters may be devitalized. Even if not hit directly, soft tissue may
be pulped, small blood vessels disrupted, and bone shattered. Large vessels may
be pushed aside, but intimal damage may lead to thrombosis. The projectile may
have enough energy to pass completely through, creating both entrance and exit
wounds of highly variable size (Figure 1.21).
•
FIGURE 1.21 High-velocity gunshot wound to the lower leg with extensive medial
bone and soft-tissue loss. The bullet passed completely through.
Although shotguns have lower muzzle velocity than rifles, the aggregate mass
of the projectiles may be 10 times greater than a single bullet, resulting in
proportionally greater wounding power, especially at close range (Figure 1.22).
Multiple projectiles that spread over a contiguous area can devitalize a large
volume of tissue. Shotguns may be loaded with various numbers and sizes of
projectiles, including bird shot (multiple small spherical projectiles), buckshot
(fewer but larger spherical projectiles), and slugs (1 large projectile). Shotgun
wounds are considered type III open fractures.
Plastic and rubber bullets from firearms and BBs or small pellets from air
guns are inaccurate low-velocity missiles that still have the potential to maim or
kill. Blank rounds of ammunition are cartridges with gunpowder but no
projectile; however, the explosive force of blank ammunition may kill or injure
at close range.
BURNS AND BLAST INJURIES

Burns cause coagulative tissue necrosis. The depth of the injury is related to the
severity and duration of the applied heat. Initially, one may see soft-tissue loss
and soft-tissue edema. Osteoporosis and periostitis may occur in the weeks that
follow. Periarticular osseous excrescences are common after extensive burns and
may be seen 2 to 3 months after injury (Figure 1.23). The range of motion of
involved joints will be limited mechanically. The exact pathogenesis of these
ossifications is unknown and seems not to correlate with the severity of the burn.
•
FIGURE 1.22 Shotgun wound to the foot.
•
FIGURE 1.23 Soft-tissue ossification at the knee following severe burns. Skin
grafting has also been performed.
Fireworks are legally available in many locales in the United States, and blast
injuries cluster around the holidays of New Year’s Eve and 4th of July.8
Fireworks contain low-order explosives, which undergo deflagration and
produce subsonic explosions. Fireworks may cause primary blast injuries,
particularly to the hands and fingers of those holding the exploding firework.
Open fractures, amputated parts, and degloving injuries are typical injuries
(Figure 1.24). Shrapnel is not found in fireworks. High-order explosives such as
TNT, ammonium nitrate fuel oil, and C-4, as might be found in military,
terrorist, or industrial explosions, undergo detonation, a nearly instantaneous
transformation that produces supersonic explosions and more serious primary
blast injuries at a greater distance. Secondary blast injuries are those caused by
flying debris and projectiles such as shrapnel; tertiary blast injuries are caused by
people being thrown through the air; and quaternary blast injuries are caused by
other results of the event, such as a building collapsing or a vehicle crashing.
•
FIGURE 1.24 Blast injury from the explosion of a handheld firework.
STRESS INJURIES
Stress fractures may be divided into fatigue fractures, in which normal bone
fractures in response to abnormal repetitive loads, and insufficiency fractures, in
which abnormal bone fractures in response to normal repetitive loads. Fractures
through focal lesions such as tumors are called pathologic fractures.
Fatigue fractures or stress fractures in normal bone are the result of repetitive
physical activity, usually occupational or recreational.9,10 The individual loads
themselves are insufficient to cause fracture, but frequent cyclic loading
stimulates remodeling, with the quality and location of the remodeling
depending on the magnitude and direction of the loading (the Wolff law). The
ultimate result is bony hypertrophy. Because cortical bone remodels by a process
of resorption and then replacement, there is a vulnerable period during increases
in physical activity when the bone has been weakened by resorption but not yet
strengthened by replacement. The level and frequency of activity determine the
duration of vulnerability. Muscular fatigue is also thought to have a role in the
generation of stress fractures. With repetitive exercise to near exhaustion of
muscles, decreased stress shielding by muscle action may increase the loads
placed on the bones. The site of a stress fracture depends on the type of activity.
In runners, for example, common sites include the metatarsal shafts, the tibial
shaft, the sesamoids of the foot, the medial femoral cortex, and the inferior pubic
ramus. Students with heavy book bags and other occupational or recreational
backpackers may sustain stress fractures involving the clavicle or upper ribs.
Stress fractures are typically identified while they are still incomplete; with rest,
the prognosis for healing is excellent.
A similar process of cyclic loading may cause insufficiency fractures, in
which abnormally weak bone fractures in response to normal loads. Such
fractures may occur, for example, in older, osteoporotic patients who suddenly
become more mobile after joint replacement surgery or in patients with
metabolic bone disease and decreasing bone strength.
•
FIGURE 1.25 Tibial stress fracture (grade 1) with periosteal edema (arrow)
demonstrated on axial STIR MRI. The marrow is normal.
•
FIGURE 1.26 Calcaneal stress fractures (grade 2). Sagittal STIR MRI shows
marrow edema within the cancellous bone of the calcaneus. Retrocalcaneal bursitis is
also present (arrow).
The severity of a stress injury along the spectrum from accelerated stress
remodeling to complete structural failure may be graded on the basis of imaging.
The earliest radiologic change is periosteal edema without marrow edema on
MRI (Figure 1.25); the bone scan may be vaguely positive, and radiographs will
be normal (grade 1). A more advanced injury will show early marrow edema on
MRI (Figure 1.26), a more focally positive bone scan, and normal radiographs
(grade 2). The next higher-grade injury will show well-established marrow
edema on MRI (both inversion recovery and T1) (Figure 1.27), a focally positive
bone scan, and sometimes a fracture line involving part of the cortex on
radiographs (grade 3). The highest grade will have a discrete fracture line or
cortical signal abnormality on MRI with surrounding edema (Figure 1.28), an
intensely positive bone scan, and sometimes a definite fracture line on
radiographs. CT may be used to demonstrate fractures or healing (grades 3 or 4).
In the absence of a discrete fracture, sometimes the involved cortex may appear
less dense on CT, a finding called graying of the cortex (Figure 1.29) that
corresponds to stress remodeling (grades 1 or 2). Stress fractures may also be
oriented longitudinally, along the long axis of the bone (Figure 1.30).11 As stress
fractures heal, fracture callus with subsequent remodeling is seen (Figure 1.31).
•
FIGURE 1.27 Second metatarsal stress fracture (grade 3). A, Axial T1 MRI shows
low signal in the marrow of the second metatarsal (arrow). B, Axial STIR MRI shows
marrow edema and surrounding soft-tissue edema (arrow).
•
FIGURE 1.28 Tibial shaft stress fracture (grade 4). Coronal T2 FS MRI shows a
focus of marrow edema traversed by a dark fracture line (arrow). Surrounding soft-
tissue edema is also present.
•
FIGURE 1.29 Tibial stress fractures with graying of the anterior cortex at multiple
foci on sagittal CT. Two of the foci are indicated by arrows.
FRACTURE DESCRIPTION
Precise use of language in describing fractures and dislocations is imperative for
patient care.12 The most important fact about a fracture is its site within the
skeleton. The location within the involved bone should be precisely noted. In the
long bones, it is conventional to divide the shaft into thirds and to indicate which
third is involved (proximal, middle, or distal). A fracture site can also be located
at the junction of the proximal and middle thirds or the junction of the middle
and distal thirds. If anatomic landmarks are present, they may be used for
reference; some anatomic regions have specific terminology.
•
FIGURE 1.30 Longitudinal stress fracture of the distal tibial shaft. A, Axial CT shows
a vague fracture line in the sagittal plane through the anterior cortex of the distal tibia,
with a small amount of periosteal and endosteal fracture callus (arrows). B,
Radionuclide bone scan shows linear activity along the distal tibial shaft.
•
FIGURE 1.31 Healing stress fracture of the second metatarsal (arrow).
The morphology of the fracture should be described in terms of the principal

fracture line: transverse, spiral, oblique, and so forth. Simple fractures have 1
fracture plane and 2 major fragments. Comminuted fractures have 2 or more
fracture planes and 3 or more major fragments. Examples of comminuted
fractures include transverse fractures with butterfly fragments and segmental
fractures (transverse fractures at different levels of a shaft that isolate a segment
of bone) (Figure 1.32).
•
FIGURE 1.32 Segmental fracture of the femoral shaft with complete displacement.
Alignment refers to the long axis of the fragments; angulation is a change

from the normal alignment and refers specifically to the angle between the long
axes of the major fragments. The direction of angulation of a fracture reflects the
direction of loading. By convention, varus or medial angulation of the distal
fragment is deviation of the distal part toward the midline of the body; valgus or
lateral angulation of the distal fragment is deviation of the distal part away from
the midline of the body. Angulation can also be anterior or posterior. An
alternative method of reporting fracture angulation is to describe the direction of
the apex of the angle formed by the major fragments. A fracture with valgus
(lateral) angulation of the distal fragment would be described as apex medial.
•
FIGURE 1.33 Dorsal proximal interphalangeal dislocation.
Position refers to the relationship of the fracture fragments to their normal

anatomic location. Loss of position is called displacement. Fragments that are
completely separated from each other are completely displaced. Fragments that
maintain partial contact with their anatomic location are partially displaced;
partial displacement of cortical fractures is usually described in terms of a
proportion of the shaft width. In nondisplaced fractures, the fragments remain in
their normal anatomic location. In rotary displacement, the fragments turn away
from each other; documentation of rotary displacement requires an image
acquisition that includes both ends of the fractured bone. Shortening is the
overlap of fragments along the axis of the limb, and distraction is the separation
of fragments along the axis of the limb.
Loss of position by articulating bones is called dislocation or luxation if there
is no remaining contact between the articulating bones and subluxation if partial
contact has been maintained. Dislocations and subluxations should be described
by the location of the distal part relative to the proximal part. For example, in a
dorsal proximal interphalangeal dislocation, the middle phalanx has dislocated to
a position that is dorsal to the proximal phalanx (Figure 1.33).
The apparent position and alignment of bones and fragments on radiographs
can vary with positioning of the part relative to the X-ray beam. In general, 2
views obtained 90° to each other is the minimum necessary to determine the
relative position and alignment of fracture fragments in 3 dimensions. Sequential
measurements of fracture position and angulation on radiographs are often not
possible unless great care is taken to obtain the radiographs in the same
projection.
•
FIGURE 1.34 Osteochondral fracture of the patella. The fracture fragment (arrow)
consists of articular cartilage with an attached segment of subchondral bone.
•
FIGURE 1.35 Axial T2 FS MRI shows a cartilage injury of the patella (arrowhead)
with loose cartilage fragment (black arrow) and medial retinaculum sprain (white
arrow). Other loose cartilage fragments and bone bruises were demonstrated on
other images (not shown).
Intra-articular fractures are those at the end of a bone in which the fracture
line extends into the articulating portion of the bone, although not necessarily
into the articular surface itself. Osteochondral fractures are intra-articular
fractures that extend through both bone and articular cartilage. On radiographs,
the presence of the cartilage fragment may be inferred from the donor site of the
bony fragment (Figure 1.34). Cartilage injuries may be imaged directly by MRI
(Figure 1.35).
Avulsion fractures are traction fractures from tensile loading of tendons or
ligaments and range from large transverse fractures to tiny flecks of cortex at the
insertion or origin of the involved muscle or tendon. These fractures indicate
disruption of the bone-tendon or bone-ligament complex and have great clinical
significance. They also imply that the soft-tissue structure—the tendon or
ligament that has pulled off the bone fragment—is itself still intact.
FRACTURE CLASSIFICATION
There are many different systems of classification for fractures in each region of
the skeleton, independently devised for different purposes by practitioners with
disparate interests.12 The best classifications are those that provide a conceptual
basis for understanding patterns of injuries, facilitate clinical management
decisions, or correlate with prognosis. Descriptive and anatomic classifications
are useful in radiology, and when both writers and readers of the radiologic
report use the same classifications in the same way, precise communication is
possible. However, for complex fracture classification systems, observer
variability may be high.13 The closest thing to a universally accepted
comprehensive fracture classification system is the Orthopedic Trauma
Association fracture and dislocation classification.14 In clinical use, the system
assigns a digit for the bone or anatomic region, a second digit for segment within
the bone or region, a letter for fracture type, a digit for fracture group, and if
needed, a second digit for fracture subgroup. For example, a segmental fracture
of the femoral shaft (see Figure 1.32) would be classified as 32-C2, where “3”
designates the femur, “2” designates the diaphysis, “C” designates the complex
fracture type, and “2” designates the segmental fracture group. The Orthopedic
Trauma Association classification system also covers dislocations. Rather than
guess the clinician’s preferred classification system and attempt to use it, the
radiologist should strive to describe the fractures in sufficient detail for any
classification system to be applied.
References
1. Amin S, Achenbach SJ, Atkinson EJ, Khosla S, Melton III LJ. Trends in fracture incidence: a
population-based study over 20 years. J Bone Miner Res. 2014;29(3):581–589. doi:10.1002/jbmr.2072
[PMID:23959594; PMCID:PMC3929546].
2. Nordin M, Frankel VH. Basic Biomechanics of the Musculoskeletal System. 4th ed. Philadelphia:
Lippincott Williams & Wilkins; 2012.
3. Mandalia V, Henson JH. Traumatic bone bruising—a review article. Eur J Radiol. 2008;67(1):54–61.
doi:10.1016/j.ejrad.2008.01.060 [Epub June 4, 2008. PMID:18534802].
4. Jacobson JA. Fundamentals of Musculoskeletal Ultrasound. 2nd ed. Philadelphia: Saunders; 2012.
5. Gustilo RB. Current concepts in the management of open fractures. Instr Course Lect. 1987;36:359–366
[PMID:3437136].
6. Halawi MJ, Morwood MP. Acute management of open fractures: an evidence-based review.
Orthopedics. 2015;38(11):e1025–e1033. doi:10.3928/01477447-20151020-12 [PMID:26558667].
7. Wilson AJ. Gunshot injuries: what does a radiologist need to know? RadioGraphics. 1999;19:1358–
1368.
8. Sandvall BK, Jacobson L, Miller EA, et al. Fireworks type, injury pattern, and permanent impairment
following severe fireworks-related injuries. Am J Emerg Med. April 25, 2017;35(10):1469–1473.
doi:10.1016/j.ajem.2017.04.053 [PMID:28495236].
9. Pathria MN, Chung CB, Resnick DL. Acute and stress-related injuries of bone and cartilage: pertinent
anatomy, basic biomechanics, and imaging perspective. Radiology. 2016;280(1):21–38.
doi:10.1148/radiol.16142305 [PMID:27322971; PMCID:PMC4942997].
10. Matcuk Jr GR, Mahanty SR, Skalski MR, Patel DB, White EA, Gottsegen CJ. Stress fractures:
pathophysiology, clinical presentation, imaging features, and treatment options. Emerg Radiol.
2016;23(4):365–375. doi:10.1007/s10140-016-1390-5 [Epub March 22, 2016. PMID:27002328].
11. Jeske JM, Lomasney LM, Demos TC, Vade A, Bielski RJ. Longitudinal tibial stress fracture.
Orthopedics. 1996;19(3):263; 66; 68; 70 [PMID:8867556].
12. Court-Brown C, Heckman JD, McQueen MM, Ricci WM, Tornetta III P, eds. Rockwood and Green’s
Fractures in Adults. 8th ed. Philadelphia: Wolters Kluwer Health; 2015.
13. Higgins LJ, Alluwaimi F, Osgood G, Wang K, Carrino JA. Avoiding miscommunication in acute
musculoskeletal trauma cases: use of standardized reporting and classification schemes. Semin
Musculoskelet Radiol. 2013;17(4):341–358. doi:10.1055/s-0033-1356464 [PMID:24101175].
14. Marsh JL, Slongo TF, Agel J, et al. Fracture and dislocation classification compendium—2007:
Orthopaedic Trauma Association classification, database and outcomes committee. J Orthop Trauma.
2007;21(10 suppl):S1–S163.
CHAPTER SELF-ASSESSMENT QUESTIONS
1. Avulsion fractures typically result from which form of biomechanical loading?

A. Bending
B. Compression
C. Tension
D. Torsion
2. Which 2 demographic groups have the highest incidence of fractures?

A. Men (age 35 years or less), women (age 35 years or less)
B. Men (age 35 years or less), women (age 60 years or more)
C. Men (age 60 years or more), women (age 35 years or less)
D. Men (age 60 years or more), women (age 60 years or more)
3. Bayonet apposition is a descriptive term that may be most appropriately

applied to which fracture type?
A. Avulsion fracture
B. Shaft fracture
C. Intra-articular fracture
D. Stress fracture
4. Which biomechanical mechanism of fracture typically results in comminution?

A. Tension
B. Torsion
C. Bending
D. Compression
Answers to Chapter Self-assessment Questions

1. C Avulsion fractures typically result from loading in tension.
2. B Young men and postmenopausal women have the highest incidence of
fractures among these demographic groups.
3. B Bayonet apposition is used to describe displaced, overlapping shaft
fractures without angulation.
4. C The bending mechanism of fracture typically results in a transverse
fracture with butterfly fragment.
2
Imaging of Upper Extremity
Fractures and Dislocations
Manickam Kumaravel, Refky Nicola, Stanislav Belchuk, and Felix S. Chew
Trauma is the most common reason for imaging the upper extremity.
Radiography is always the initial study performed, sometimes supplemented by
CT or MRI.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of upper extremity fractures and
dislocations, the learner will be able to
3. summarize relevant concepts and knowledge for the following anatomic regions: hand, wrist,
distal radius and forearm, elbow, shoulder and arm, clavicle, acromioclavicular (AC) joint,
sternoclavicular joint, and thoracic cage.
FINGERS
Metacarpal and phalangeal fractures are among the most common skeletal
injuries in the general population. Approximately 78% of hand fractures occur in
males, with peak incidence in young men.1
Avulsion injuries of the phalanges are caused by the tensile failure of the
ligamentous or musculotendinous units. These injuries result when excessive
loading occurs while the tendon or ligament is already under tension. The
substance of a tendon or ligament may tear, or there may be avulsion of its bony
insertion. For example, sudden, forcible flexion of the distal interphalangeal
(DIP) joint of an extended finger, as occurs when an outstretched finger is struck
by a baseball, may result in tensile failure of the extensor mechanism of the
distal phalanx. The injury is called a baseball finger, and the resulting clinical
deformity is called a mallet finger, in which the DIP joint is maintained in
flexion and cannot be extended (Figure 2.1).2 An avulsion fracture of the dorsal
proximal corner of the distal phalanx is present in 25% of cases of baseball
finger; thus, most of these injuries are tendinous. An avulsed bone fragment can
be retracted by muscle pull (Figure 2.2).
The converse injury occurs with forcible extension of the DIP joint of a
flexed finger or with forcible hyperextension at the DIP joint. In this case, the
volar plate of the distal phalanx at the flexor digitorum profundus tendon
insertion may be avulsed; alternatively, the tendon may tear. Similar injuries may
occur at the proximal interphalangeal (PIP) joint.
Purely ligamentous and tendinous injuries are more common than bony
avulsions in the fingers; therefore, radiographs may show only soft-tissue
swelling or deformities of alignment. Avulsion fractures at the base of a phalanx
from the volar edge indicate disruption of the attachment of the volar plate.
Avulsions from the lateral edge indicate disruption of the attachments of
collateral ligaments (Figure 2.3). Avulsions from the dorsal edge indicate
disruption of the extensor tendon. The avulsed fragments always contain the
tendinous or ligamentous insertion (enthesis) and may range in size from a tiny
sliver of cortical bone to a large intra-articular fragment.
If the intra-articular fragment involves one-third3 or more of the articular
surface or volar subluxation resulting in joint incongruency, the joint may
subluxate (Figure 2.4) and require operative treatment.
In contrast to fracture fragments, accessory ossicles and sesamoid bones
invariably are completely corticated, and no donor site should be present.
Deformities of alignment reflect the function of the injured unit. In some cases,
stress views may be necessary to demonstrate the loss of function.
The most common dislocation occurs at the PIP joint (Figure 2.5).4
Nonmedical personnel often reduce PIP joint dislocations, and many fracture-
subluxations are actually reduced fracture-dislocations. After reduction, if there
are no fractures, one may see only soft-tissue swelling. Dorsal dislocations are
common, lateral dislocations are less common, and volar dislocations are rare.
Dorsal dislocations, most commonly of the middle finger, imply injury of the
volar plate (with or without avulsion fractures), both collateral ligaments and the
dorsal joint capsule. Lateral dislocations are unstable because of interposition of
the collateral ligament and/or lateral band in the joint, which results in
radiographic widening of the joint and instability on examination. Volar
dislocations are uncommon. However, when these do occur, they result in
disruption of the extensor tendon central slip.
•
FIGURE 2.1 Mallet finger resulting from extensor tendon rupture.
•
FIGURE 2.2 Mallet finger fracture with displacement of the dorsal fragment.
Fractures of the distal phalanges are common and typically result from direct
impact or crushing mechanisms (Figure 2.6). Phalangeal tuft fractures may also
be associated with subungual hematoma. When the germinal matrix is involved,
the nail should be removed and a repair should be performed to prevent a nail
deformity.
The most common metacarpal fracture is an extra-articular impacted fracture
of the fifth metacarpal neck with volar angulation (Figure 2.7). In severe cases,
the fourth metacarpal neck may also be fractured. The metacarpal neck
comprises the weakest area of the bone. It is sustained by bending and axial
loading when the closed fist strikes an object (eg, a wall or chin). This fracture
of the neck of the metacarpal is commonly called the boxer’s fracture.
•
FIGURE 2.3 Avulsion fracture at the collateral ligament insertion of the middle
phalanx (arrow). The soft tissues are swollen.
•
FIGURE 2.4 Avulsion fracture of the dorsal margin of the distal phalanx at the distal
interphalangeal joint with anterior subluxation of the major fragment (arrow). The
major fragment includes approximately one-third of the articular surface, with the
remainder on the dorsal avulsion fragment.
THUMB
Ligamentous disruption of the ulnar collateral ligament of the thumb’s
metacarpophalangeal joint, or gamekeeper’s thumb, may be sustained during
downhill skiing when an improperly planted pole places sudden valgus stress on
the thumb.5 Similar mechanisms of injury may also occur in sports such as
football, hockey, wrestling, and basketball. Unless there is avulsion of a
fragment of bone, stress views may be necessary to show this injury on
radiographs (Figure 2.8). This occurs because of the violent hyperabduction of
the thumb. Rupture of the ulnar collateral ligament can be either total or partial
and usually occurs at the distal point of insertion.
•
FIGURE 2.5 Dorsal dislocation of the proximal interphalangeal joint.
•
FIGURE 2.6 Crush injury of the distal phalanx with an open fracture involving the
tuft.
The exceptional mobility of the thumb in opposing the other digits is possible
in part because of the lack of bony constraints at the carpometacarpal joint and
the lack of ligamentous attachments to the other metacarpals, thus allowing for
precise fine motor skills such as pinch and opposition. This also occurs because
of the shallow saddle-shaped articulation between the first metacarpal and the
trapezium. Axial loading of a partially flexed first metacarpal can produce a
simple intra-articular fracture. The adductor pollicis and abductor pollicis longus
muscles pull the metacarpal base and shaft proximally, but the anterior lip
remains attached to the trapezium by its ligaments (Bennett fracture) (Figure
2.9). A Bennett fracture is a 2-part fracture-dislocation in which the entire thumb
metacarpal is subluxated dorsally, radially, and proximally by the pull of the
abductor pollicis longus. These intra-articular fractures usually require operative
reduction and fixation.6,7 If a T- or Y-shaped comminuted fracture (Rolando
fracture), rather than a simple fracture, is sustained, anatomic reduction and
fixation may become more problematic (Figure 2.10). In contrast to these
injuries, extra-articular fractures of the first metacarpal shaft present few
problems in management because muscle origins along the length of the shaft
prevent displacement.
•
FIGURE 2.7 Boxer’s fracture of the fifth metacarpal neck.
•
FIGURE 2.8 Avulsion fracture (arrow) at the proximal phalanx of the thumb by the
ulnar collateral ligament (gamekeeper’s thumb).
WRIST
The wrist positions the hand in space, transmits power to the hand from muscles
in the forearm, and transmits mechanical force between the hand and the
forearm. Its range of motion is magnified in flexion and extension and in radial
and ulnar deviation by a dual articulation: one between the radius and lunate and
one between the lunate and capitate. With ulnar and radial deviation of the hand,
the distal carpal row rotates and turns. The carpus can be envisioned as having a
central column that consists of the lunate and the capitate. Flexion and extension
and the transmission of mechanical force occur through the central column. The
capitate, distal carpal row, and hand comprise a single functional unit. The lunate
is an intercalated segment between the capitate and the radius that has no direct
muscular control (no muscles insert on the lunate). The scaphoid flanks the
lunate on one side and functions as a connecting rod alongside the capitate and
lunate, providing stability during motion. The triquetrum acts as a pivot for
intercarpal rotation through a sloping, helicoid articulation with the hamate.
•
FIGURE 2.9 Bennett fracture. An intra-articular fracture of the base of the first
metacarpal with dislocation. The small medial fragment (arrow) maintains its
attachment to the joint, whereas the metacarpal has dislocated proximally.
•
FIGURE 2.10 Rolando fracture. T-shaped fractures (arrow and arrowheads) at the
base of the first metacarpal shown by coronal CT.
•
FIGURE 2.11 Ligaments of the wrist. The strong ligaments are on the volar aspect
of the wrist and form a sling that suspends the carpus from the distal forearm. The
space of Poirier exists because there is no strong ligamentous attachment of the
capitate to lunate. Many indirect injuries of the carpus involve a carpal sling disruption
that extends into the space of Poirier.
•
FIGURE 2.12 Scaphoid waist fracture. A, The fracture is not visible on the standard
posteroanterior radiograph. B, The special scaphoid radiograph shows the fracture
(arrow). The wrist is placed in ulnar deviation and the X-ray beam is angled 20° to 30°
off vertical, from the hand toward the radius.
Ligaments of the wrist limit motion when they become taut at their maximum
excursion. The volar carpal ligaments are strong and form a sling that suspends
the carpus from the radius and triangular fibrocartilage complex (TFCC) (Figure
2.11). The dorsal ligaments are weaker. Interosseous ligaments bind adjacent
carpal bones to each other; those of clinical importance are the scapholunate and
lunotriquetral ligaments. The scaphoid and triquetrum flank the lunate on either
side and have strong ligamentous attachments to the distal carpal row and
attachments to the lunate and to the distal forearm. Because no strong ligaments
connect the capitate and lunate to each other, the stability of this articulation
depends on the integrity of the adjacent scaphoid and triquetrum and their
ligamentous attachments. The gap in the volar ligamentous sling at the lunate-
capitate articulation is called the space of Poirier.
Radiographic evaluation of the wrist is based primarily on the appearance of
each bone and its relationship with the other bones. The arcs made by the
proximal articular surfaces of the proximal carpal row, the distal articular
surfaces of the proximal carpal row, and the proximal articular surfaces of the
distal carpal row are helpful anatomic landmarks.8 The positions of the scaphoid
fat stripe and the pronator quadratus fat pad are occasionally helpful indirect
signs of wrist fracture.
SCAPHOID
The scaphoid is divided into 3 parts: proximal third, middle third, and distal
third. The waist of the scaphoid refers to the junction of the middle and distal
thirds. Fractures of the scaphoid occur most frequently from a fall on an
outstretched hand with forced dorsiflexion of the wrist.9 Scaphoid fractures
account for approximately 85% of all isolated carpal bone fractures and are
common in young men. Most scaphoid fractures have no comminution (70% of
cases). Less common are fractures through the proximal (10%) or distal (20%)
poles. Many scaphoid fractures are nondisplaced and difficult to recognize
without special scaphoid views (Figure 2.12). The scaphoid bridges the lunate-
capitate articulation. With extreme, forceful dorsiflexion between the lunate and
capitate and perhaps impingement of the scaphoid on the dorsal radial rim, the
scaphoid starts to bend, and the fracture line begins on its volar aspect under
tensile loading, propagating transversely through the narrowest region (the
scaphoid waist). The scaphoid may also fracture during perilunate injuries
(discussed later in this chapter). Indirect signs of scaphoid fractures are
obscuration or lateral displacement of the scaphoid fat stripe and soft-tissue
swelling over the dorsum of the wrist. MRI or CT may demonstrate
radiographically occult fractures of the scaphoid and other carpal bones.10
Because the blood supply to the proximal pole of the scaphoid enters the distal
pole and courses proximally across the waist, posttraumatic osteonecrosis of the
proximal pole with nonunion is a common complication seen in up to 30% of
cases. Osteonecrosis of the scaphoid may be suggested by relative sclerosis of
the osteonecrotic fragment, which fails to participate in the regional acute
osteoporosis that accompanies fracture healing (Figure 2.13). Wrist instability,
persistent pain, and degenerative arthropathy are common sequelae of scaphoid
nonunion.
•
FIGURE 2.13 Scaphoid nonunion (short arrow) and osteonecrosis of the proximal
pole fragment (long arrow) of a scaphoid waist fracture demonstrated by coronal CT.
OTHER ISOLATED CARPAL BONES
Isolated fractures of carpal bones other than the scaphoid are relatively
uncommon.9 Isolated triquetral fractures usually involve the dorsal surface and
are seen best on lateral or slightly oblique radiographs (Figure 2.14). The dorsal
surface of the triquetrum may be fractured by means of impingement from the
ulnar styloid, shear forces, or avulsion from the strong ligamentous attachments.
Isolated lunate fractures usually involve the dorsal or volar surface and are
ligamentous avulsions. Pisiform fractures may occur with direct trauma (blow)
and are best seen on oblique radiographs. The injury can be either a vertical or
transverse fracture (linear or comminuted) or a compression injury. These
fractures can be difficult to detect on standard radiographs, and carpal tunnel or
pisotriquetral radiograph or CT or MRI images are often needed. Hamate
fractures may involve any part, but fractures of the hook of the hamate become
displaced by the insertion of the transverse carpal ligament. Hook of hamate
fractures can be identified by the disruption of the “ring” formed by the base of
the hook of the hamate, called the Signet ring sign (Figure 2.15). Complications
include nonunion, osteonecrosis, and ulnar or median nerve injury, and most are
treated surgically. Dorsal fracture-dislocations of the hamate may also occur at
the articulation of the hamate with the bases of the fourth and fifth metacarpals
(Figure 2.16).
•
FIGURE 2.14 Triquetral fracture. Lateral radiograph shows displaced avulsion
fragment (arrow) with overlying soft-tissue swelling.
PERILUNATE INJURIES
A consistent pattern of injuries is sustained around the lunate when the hand is
extended to break a backward fall.11 On impact, the hand and wrist undergo
hyperextension, ulnar deviation, and intercarpal supination (rotary motion
between the proximal and distal carpal rows). The ligamentous sling of the
carpus is loaded in tension from the radial side, and a sequence of injuries may
ensue (Table 2.1). In stage 1, rupture of the scapholunate interosseous ligament
results in separation of the scaphoid from the lunate (called scapholunate
dissociation) and volar rotation of the scaphoid about its short axis (called rotary
subluxation of the scaphoid). Both terms are used to indicate the same injury.
Radiographic findings include a widened scapholunate interval and an increased
scapholunate angle (Figure 2.17). This mechanism of loading may also fracture
the scaphoid. In stage 2, perilunate dislocation, the capitate dislocates from the
lunate dorsally, taking with it the hand and the scaphoid (Figure 2.18). The space
of Poirier opens on the radial side, often through a scaphoid fracture between the
ligamentous attachments to the capitate and lunate, but the triquetral ligaments
remain intact. In stage 3, midcarpal dissociation or triquetral dislocation, under
continued loading the triquetral ligaments fail by tear or avulsion of insertions,
separating the triquetrum from the lunate. Although the lunate remains in place,
the rest of the carpus is dislocated dorsally, coming to rest on the dorsal surface
of the lunate. The lunate is subluxated and tilted volarly but is not completely
dislocated (Figure 2.19). Lunate dislocation (stage 4) occurs if there is sufficient
force to tear the dorsal radiocarpal ligament, allowing the dorsally dislocated
carpus to eject the lunate from the radius volarly. The capitate comes to rest in
the radial articular surface. The dislocated lunate is also rotated 90° volarly, still
held to the radius by its volar ligaments (Figure 2.20). Avulsion fractures instead
of ligamentous ruptures may occur, including avulsion and tension fractures of
the carpal bones (especially the scaphoid) and of the distal radius and ulna. The
radiographic signs of reduced perilunate injuries may be subtle, particularly in
the absence of bony involvement.
•
FIGURE 2.15 The hook of the hamate fracture. A, Posteroanterior radiograph
shows disruption of the ring formed by the hook of the hamate (arrow). B, Sagittal CT
confirms the fracture (arrow).
•
FIGURE 2.16 Fracture-dislocation involving the hamate. A, Radiograph shows
dorsal fracture-dislocation (arrow) involving the articulations of the fourth and fifth
metacarpals with the hamate. B, Axial CT scan shows the displaced, comminuted
hamate fracture (arrow).
Table 2.1 PERILUNATE INJURIES OF THE WRIST
Stage Injury
1 Rotary subluxation of the scaphoid (scapholunate dissociation)
2 Perilunate dislocation
3 Midcarpal dissociation (triquetral dislocation)
4 Lunate dislocation
CARPAL INSTABILITY
The seriousness of ligamentous injuries of the wrist is often overlooked during
the acute clinical presentation, particularly if fractures are absent and
dislocations have been reduced.12 When untreated, patients with “wrist sprains”
often return with chronic, disabling wrist symptoms, including instability, pain,
decreased grip strength, posttraumatic arthritis, and painful “clicks.” Fractures of
the distal radius may be associated with more serious carpal dysfunction that
becomes apparent once the radial fractures have healed.
In dorsiflexion instability (also called dorsal intercalated segment instability),
the axes of the radius, lunate, and capitate assume a zigzag configuration with
dorsal angulation of the lunate (relative to the radius) and volar angulation of the
capitate (relative to the lunate).
In volar flexion instability (also called volar intercalated segment instability),
the zigzag is the reverse, with volar angulation of the lunate (relative to the
radius) and dorsal angulation of the capitate (relative to the lunate) (Figure 2.21).
Deformities of dorsal intercalated segment instability and volar intercalated
segment instability will lead to pain and instability if not treated appropriately.
DISTAL RADIUS AND FOREARM

Fractures of the distal radius usually occur from falls on the outstretched hand. A
Colles fracture is a nonarticular transverse fracture of the distal radial
metaphysis with dorsal displacement, dorsal angulation, and dorsal impaction
(Figure 2.22). This injury—common in older persons with osteoporosis,
particularly women—is sustained during a fall forward onto an outstretched,
dorsiflexed hand with the impact force aligned to the long axis of the radius. The
fracture results from tensile failure of the cancellous metaphyseal bone on the
volar side and compressive failure on the dorsal side. The distal radial articular
surface and the carpus are spared. In 60% of cases, the ulnar styloid is avulsed
by the TFCC. Alternatively, the TFCC may tear, the distal radioulnar joint may
dislocate, or the distal ulnar shaft may fracture. Because the radial fracture
traverses the spongy bone of the metaphysis, healing is generally prompt with
closed treatment, but associated ulnar styloid fractures frequently do not unite.
Residual, posttraumatic dorsal tilt of the distal radial articular surface may result
in instability of the wrist. A transverse radial metaphyseal fracture in which the
distal fragment is displaced and angulated volarly may be called a reverse Colles
fracture or a Smith fracture.
Simple intra-articular fractures with comminution of the distal radius that
involve either its dorsal or volar margin are called Barton fractures.
•
FIGURE 2.17 Rotary subluxation of scaphoid. A, Lateral radiograph shows volar
rotary subluxation of the scaphoid. The scapholunate angle is nearly 90°. B,
Posteroanterior radiograph shows foreshortening of the scaphoid with a cortical ring
sign over its distal pole. C, Scapholunate angle measurement. Normal scapholunate
angle is 30° to 60°.
Complex intra-articular fractures of the distal radius may be caused by high-

energy axial compression forces transmitted through the lunate to the medial half
of the radial articular surface.13 The articular surface usually splits into 3 major
fragments: the radial styloid and 2 medial fragments, 1 dorsal and 1 volar
(Figure 2.23). The medial fragments may be angulated dorsally or volarly,
depending on the degree of flexion or extension of the wrist at the time of injury.
Additional impaction and comminution may be present depending on the
magnitude of the loading. Most patients with these fractures also have
intracarpal soft-tissue injuries, including ligament tears and TFCC injuries. The
distal radioulnar joint is disrupted, and the ulnar styloid may be fractured. These
injuries are typically treated surgically.
Isolated avulsion fractures of the radial styloid may follow avulsions of the
radial collateral ligament. Compressive forces transmitted through the scaphoid
may cause isolated shear fractures of the radial styloid; these may be associated
with avulsion fractures of the ulnar styloid. Simple intra-articular fractures of the
distal radius that involve the radial styloid process are sometimes called
Hutchinson or chauffeur’s fractures (Figure 2.24).
•
FIGURE 2.18 Transscaphoid perilunate dislocation. A, Lateral radiograph shows
complete dorsal dislocation of the capitate with normal location of the lunate. B,
Posteroanterior radiograph shows the overlap of the scaphoid and capitate, but not
the triquetrum. The scaphoid is fractured. The ulnar styloid is fractured.
•
FIGURE 2.19 Midcarpal dislocation. A, Lateral radiograph shows complete dorsal
dislocation of the capitate and volar subluxation of the lunate. B, Posteroanterior
radiograph shows separation of the scaphoid, capitate, and triquetrum from the
lunate. Avulsion fractures of the triquetrum and radial styloid are present.
Dislocation or subluxation of the distal radioulnar joint may occur in

association with other fractures of the radius or in isolation. Because this injury
is often overlooked and difficult to document on radiographs, CT may be
required for the definitive diagnosis (Figure 2.25). Often, an unstable distal
radioulnar joint reduces in neutral or supination and subluxates in pronation. A
CT scan can better identify and demonstrate the presence of a distal radioulnar
dislocation, when performed in pronation and supination. Chronic dislocation or
instability of the distal radioulnar joint may result in posttraumatic wrist
disability.
•
FIGURE 2.20 Lunate dislocation. A, Lateral radiograph shows volar dislocation of
the lunate with 90° rotary displacement. The capitate occupies the normal position of
the lunate. B, Posteroanterior radiograph shows the lunate as an overlapping
triangular structure.
•
FIGURE 2.21 Carpal instability patterns on sagittal CT (different patients) (C,
capitate; D, dorsal aspect; R, radius; V, volar aspect). A, Dorsal intercalated segment
instability with capitate subluxation. The lunate (arrow) is tilted dorsally. B, Volar
intercalated segment instability. The lunate (arrow) is tilted volarly.
Most fractures of the forearm (60%) involve both the radius and ulna. Less
common are isolated fractures of the ulna with or without radial dislocation
(25%), and the least common are isolated fractures of the radius with or without
ulnar dislocation (15%). The greater the loading, the more likely it is that both
bones are fractured. Raising the forearm to ward off a blow by a blunt
instrument, such as a nightstick, may result in a tapping fracture from direct
loading of the ulnar shaft.
A fracture of the radial shaft with dislocation of the distal radioulnar joint is
called a Galeazzi fracture-dislocation (Figure 2.26). An impacted or comminuted
fracture of the radial head with dislocation of the distal radioulnar joint is called
an Essex-Lopresti fracture (Figure 2.27). A fracture of the ulnar shaft with
dislocation of the radial head is called a Monteggia fracture (Figure 2.28).
The most common type of Monteggia fracture is an angulated fracture of the
proximal ulnar shaft with apex anterior along with anterior dislocation of the
radial-capitellar joint. Less common types may also occur, including apex
posterior angulation of the ulnar shaft fracture with posterior radial head
dislocation, apex lateral angulation of the ulnar shaft fracture with lateral
dislocation of the radial head, or a combination that includes a radial head
fracture.
•
FIGURE 2.22 Transverse fracture of the distal radial metaphysis with dorsal
displacement and angulation in an elderly woman (Colles fracture). A, Lateral
radiograph. B, Posteroanterior radiograph.
•
FIGURE 2.23 Comminuted intra-articular distal radius fractures. A, Posteroanterior
radiograph shows involvement of the radiocarpal and distal radioulnar joint surfaces.
B, Lateral radiograph shows dorsal impaction and dorsal angulation of the distal
fragment.
ELBOW
The most common elbow fractures in adults involve the radial head or neck.14
Radial head and neck fractures are sustained during falls onto an outstretched
hand, impacting the radial head against the capitellum. One of the two types of
fractures is typically sustained: a linear shear fracture through the radial head
(Figure 2.29) or an impaction fracture of the radial neck (proximal radial
metaphysis) (Figure 2.30). Because they are intra-articular, a fat pad sign is often
present. Approximately half of these fractures are nondisplaced and may require
oblique views for demonstration. More severe fractures have displacement and
comminution and may also involve the capitellum.
An intra-articular olecranon process fracture may be caused by a fall onto an
outstretched hand with the elbow in flexion. The combination of axial
compression with tension from contraction of the triceps produces oblique or
transverse fractures through the semilunar notch (Figure 2.31). Fractures may
also be caused by direct falls onto the flexed elbow.
•
FIGURE 2.24 Intra-articular fracture of the radial styloid process demonstrated
using an oblique radiograph. Sometimes, these fractures are not visible on
posteroanterior and lateral radiographs.
•
FIGURE 2.25 Subluxation of the left distal radioulnar joint demonstrated by CT. A,
In supination, the joint is normally located. B, In pronation, the ulna is dorsally
subluxated (arrow).
•
FIGURE 2.26 Galeazzi fracture-dislocation. An angulated, displaced fracture of the
distal radial shaft at the junction of the middle and distal thirds with dislocation of the
distal radioulnar joint.
•
FIGURE 2.27 Essex-Lopresti fracture. A, Posteroanterior view of the wrist shows
dislocation of the distal radioulnar joint and a perilunate injury. B, Anteroposterior view
of the elbow shows a comminuted radial head fracture (arrow).
•
FIGURE 2.28 Apex anterior fracture of the ulnar shaft with anterior dislocation of the
radial-capitellar joint (Monteggia fracture, Bado type 1).
•
FIGURE 2.29 Nondisplaced radial head fracture (arrow) with anterior and posterior
fat pad signs (arrowheads).
Most acute dislocations of the elbow result from falls or sports-related

mishaps. Typically, the ulna dislocates posteriorly relative to the humerus, taking
the radius with it. In many cases, there are no associated fractures. When
fractures are associated with elbow dislocations, the fragments are often
avulsions from the coronoid process of the ulna (Figure 2.32). The size of the
coronoid fractures may affect the postreduction the stability of the elbow.
Although posterior elbow dislocations are the most common (Figure 2.33),
dislocation in other directions also may occur.
Intercondylar fractures of the distal humerus involve impaction of the ulna
into the trochlear groove, where it splits the distal humerus like a wedge, often
separating the medial and lateral fragments with a T- or Y-shaped fracture line
(Figure 2.34). Comminution and displacement are common. These fractures are
treated with open reduction and internal fixation.
Injuries in the region of the elbow can easily compromise the function of the
ulnar nerve and therefore should be evaluated both by imaging and clinical exam
for its integrity.
•
FIGURE 2.30 Impacted radial neck fracture (long arrow) with anterior and posterior
fat pad signs (arrowheads).
•
FIGURE 2.31 Intra-articular fracture of the olecranon process (long arrow). An
elbow effusion is present with fat pad sign (short arrow).
•
FIGURE 2.32 Coronoid process fracture. A, Lateral radiograph shows fracture
fragments (arrow). B, Sagittal CT shows the fragments and the donor site.
HUMERUS
Fractures of the proximal humerus usually occur through the shaft at the surgical
neck (Figure 2.35). The rotator cuff abducts and rotates the proximal fragment.
The greater or lesser tuberosities may also be fractured, and in severe injuries,
the anatomic head may be dislocated. Anatomic neck fractures are rare and have
a poor prognosis because the blood supply to the humeral head is disrupted.
Fractures of the humeral shaft are laterally and posteriorly angulated when the
fracture separates the insertions of the pectoralis major and the deltoid, allowing
the pectoralis major to adduct the proximal fragment. A fracture below the
deltoid insertion allows it to abduct the proximal fragment, resulting in medial
angulation. Most simple humeral shaft fractures are treated by closed means;
occasionally, screws, plates, or rods are used.
•
FIGURE 2.33 Posterior elbow fracture-dislocation. A, Lateral radiograph shows the
dislocated radius and ulna. The posterior fat pad (arrow) is displaced by distortion of
the capsule. B, Anteroposterior radiograph shows the proximal radioulnar joint is
intact.
•
FIGURE 2.34 Intercondylar fracture of the distal humerus. A, Anteroposterior
radiograph shows distal humerus fractures with displaced medial and lateral
condyles. B, Coronal CT shows a comminuted T-shaped fracture.
An isolated fracture of the greater tuberosity may occur in falls or other types
of trauma. Because the supraspinatus and infraspinatus tendons of the rotator
cuff have their insertion on the greater tuberosity, patients may present with
signs and symptoms of rotator cuff tears (Figure 2.36). Another unusual type of
fracture involving the humerus is the avulsion fracture of various structures that
attach to the humerus, including ligaments and tendons (Figure 2.37). MRI is
often necessary to evaluate the soft-tissue structures in such cases (see chapter
6).
•
FIGURE 2.35 Surgical neck fracture of the humerus. A, External rotation. B, Internal
rotation. Fracture is seen to extend from the medial to the lateral cortical margins
(arrows) with impaction.
GLENOHUMERAL JOINT DISLOCATIONS

In the acute setting, radiographs and CT are the primary means of imaging the
shoulder.15 Because the articular surface of the glenoid is oriented obliquely, the
radiographic examination should always include a lateral view (axillary,
transscapular, or transthoracic) when shoulder dislocation is suspected. In
approximately 95% of cases of glenohumeral dislocation, the humeral head
dislocates anteriorly and ends up anterior, inferior, and medial to the glenoid
process in a subcoracoid location (Figures 2.38 and 2.39). Abduction and
external rotation of the arm cause the acromion to come in contact with the
surgical neck of the humerus, and the humeral head can be levered out of the
glenoid fossa. A direct blow to the back of the shoulder can eject the humeral
head, and traction on the limb can pull it out. Impaction of the anterior-inferior
surface of the glenoid labrum on the posterolateral aspect of the humeral head
after it dislocates may cause a depressed humeral head fracture called the Hill-
Sachs lesion (Figure 2.40). Less dramatic but perhaps more important than the
dislocation itself is the concomitant detachment of the labrum and capsule from
the anterior glenoid process (Bankart lesion), sometimes associated with an
avulsion fracture (bony Bankart lesion) (see chapter 6). These injuries often
result in posttraumatic anterior shoulder instability or recurrent dislocations.
In approximately 5% of shoulder dislocations, the humeral head comes to rest
posterior to the glenoid process, and the dislocation may be difficult to recognize
on standard anteroposterior views (Figure 2.41). An impaction fracture of the
anterior aspect of the humeral head may be present and is called reverse Hill-
Sachs lesion (Figure 2.42). Posterior shoulder dislocations may occur in the
setting of tonic-clonic seizures. Other types of shoulder dislocations are rare.
Acute dislocations are treated with closed reduction; associated soft-tissue or
glenoid rim injuries may require surgical repair.
Postreduction views are mandatory for the evaluation of the anterior-inferior
glenoid as the bony Bankart injuries of the anterior-inferior glenoid are
visualized in 35% of cases.
CLAVICLE
Fractures of the clavicle usually occur in the middle third, medial to the
coracoclavicular (CC) ligaments (Figures 2.43 and 2.44). The
sternocleidomastoid muscle displaces the proximal fragment superiorly, and the
shoulder, acting through the CC ligament, displaces the distal fragment
inferiorly. Clavicle fractures may be treated with open reduction and internal
fixation or conservatively. Clavicular fractures distal to the CC ligaments may be
complicated by tears of the CC ligaments or avulsion of the coracoid process.
Fractures of the medial clavicle may be difficult to identify on radiographs.
ACROMIOCLAVICULAR JOINT
AC injuries involve the disruption of the AC and CC ligaments (shoulder
separation).16 The inferior surfaces of the acromion process and the distal
clavicle are normally at the same level on anteroposterior radiographs. In type I
injury, the AC ligaments are stretched but not disrupted, and radiographs are
normal or show a slight increase in the joint space. When the AC ligaments are
completely torn but the CC ligaments are stretched but functionally intact, the
distal clavicle subluxates superiorly (type II). If both AC and CC ligaments are
torn (type III), the clavicle dislocates and the space between clavicle and
coracoid process widens. Other types of AC injuries are rare. Complete AC and
CC ligament disruption with posterior displacement of the clavicle into the
trapezius is considered type IV (Figure 2.45). Type V is a severe form of type III,
with complete AC and CC ligament disruption with marked superior
displacement of the clavicle, typically greater than one shaft width (Figure 2.46).
Type VI is the inferior dislocation of the distal clavicle and is extremely rare.
MRI may be helpful in demonstrating AC injuries (see chapter 6).
•
FIGURE 2.36 Greater tuberosity fracture. A, Anteroposterior radiograph shows a
fragment of the greater tuberosity displaced superior to the humeral head (arrow). B,
The Y-view shows the humeral head to be normally located. The fragment (arrow) is
from the posterior aspect of the greater tuberosity, corresponding to the insertion of
the infraspinatus tendon. C, Coronal CT shows the fragment (long arrow) and the
donor site (short arrow).
STERNOCLAVICULAR JOINT
Dislocations of the sternoclavicular joint are usually sustained in high-speed
motor vehicle collisions. Although radiographs may demonstrate superior
dislocations, CT may be required to demonstrate a posterior dislocation (Figure
2.47). Anterior dislocations of the sternoclavicular joint are more common than
posterior dislocations, but the latter have more serious potential complications,
including compromise of the great vessels and airway.
THORACIC CAGE
Blunt chest trauma sustained in motor vehicle collisions may crush the bony
thorax on direct impact. Pulmonary contusion, pneumothorax, myocardial
contusion, diaphragmatic rupture, and abdominal injuries may result. The sudden
deceleration that accompanies direct impact may cause transection of the
thoracic aorta.
Rib fractures may occur from direct blows or crush injuries (Figure 2.48).
Oblique views of the chest are often necessary to demonstrate fractures of the
ribs because of their arcuate course. Rib fractures may be difficult to see initially
but are more obvious later as they become displaced by constant respiratory
motion. Knowing the sites of maximal pain and point tenderness is helpful. Rib
fractures may be multiple, in which case they involve adjacent ribs in a linear
array. A flail chest occurs when there are multiple rib fractures that isolate a
segment of the chest wall and cause paradoxic motion with respiration.
Complications and associated conditions include pulmonary contusion,
pneumothorax, hemopneumothorax, hemothorax, tracheal or bronchial tear, and
interstitial emphysema. Fractures of the first 3 ribs usually follow severe trauma.
The most common rib fractures are of the posterior or lateral aspects of the
fourth through ninth ribs. Fractures of the lower ribs may be associated with
visceral injuries. A rib may fracture with violent coughing or sneezing, usually at
the anterior aspect along the diaphragmatic insertion. Stress fractures may also
occur at the insertions of the serratus anterior muscles (first through ninth ribs)
or scalene muscles (first and second ribs). Rib fractures that occur without
trauma or with minimal trauma raise suspicion for a pathologic fracture.
•
FIGURE 2.37 Bony humeral avulsion of the inferior glenohumeral ligament lesion.
Coronal CT shows a linear bone fragment (arrow) medial to the proximal humerus.
•
FIGURE 2.38 Anterior shoulder dislocation. A, Anteroposterior radiograph shows
the humeral head dislocated medially and inferiorly. B, Axillary radiograph shows the
humeral head dislocated anteriorly.
FIGURE 2.39 • Anterior shoulder dislocation demonstrated on transscapular
radiograph (“Y-view”).
The sternum fractures with severe trauma, such as a direct impact on the chest
from the steering wheel in a high-speed motor vehicle crash. Most sternal
fractures are transversely oriented through the body of the sternum or the
sternomanubrial junction (Figures 2.49 and 2.50). Hyperflexion of the thoracic
cage is another mechanism of sternal fracture and may occur in association with
thoracic spine wedging fractures during falls.
•
FIGURE 2.40 Hill-Sachs lesion. Anteroposterior radiograph of the shoulder with the
humerus internally rotated shows an impaction fracture (arrow) of the humeral head,
which was sustained during a previous anterior dislocation.
•
FIGURE 2.41 Posterior shoulder dislocation. A, Anteroposterior radiograph shows
internal rotation of the humeral head. B, The Y-view shows posterior position of the
humeral head relative to the glenoid fossa.
•
FIGURE 2.42 Posterior shoulder dislocation with impaction fracture of anterior
humeral head (reverse Hill-Sachs lesion).
•
FIGURE 2.43 Comminuted midshaft clavicular fracture with superior displacement
of the medial fragment. The position of the distal fragment is maintained by the intact
coracoclavicular ligaments.
•
FIGURE 2.44 Distal clavicle fracture. The inferior fragment (long arrow) is attached
to the coracoid process by the intact coracoclavicular ligament. The distal fracture
(short arrow) is minimally displaced.
•
FIGURE 2.45 Acromioclavicular (AC) separation (type II). Angled radiograph of
both AC joints shows subluxation on the left (arrow), normal on the right.
•
FIGURE 2.46 Acromioclavicular separation (type V) (arrow).
•
FIGURE 2.47 Posterior-superior dislocation of the right sternoclavicular joint. A,
Radiograph shows medial position of the right clavicular head (arrow). B, Axial CT
scan shows posterior dislocation (arrow). C, Coronal reconstruction from CT scan
shows superior dislocation (arrow).
•
FIGURE 2.48 Fractures of left ribs 4 through 7 (arrows) sustained in a high-speed
automobile crash.
•
FIGURE 2.49 Manubrium fracture. A, Lateral radiograph and B, sagittal reformatted
CT show nondisplaced fracture (arrows) of the manubrium.
•
FIGURE 2.50 Sternal body fracture. Axial CT shows a nondisplaced fracture (arrow)
through the body of the sternum.
References
1. Zhang Y. Clinical Epidemiology of Orthopaedic Trauma. 2nd ed. New York: Thieme; 2016.
2. McMinn DJ. Mallet finger and fractures. Injury. 1981;12(6):477–479 [PMID:7275291].
3. Calfee RP, Sommerkamp TG. Fracture-dislocation about the finger joints. J Hand Surg Am.
2009;34(6):1140–1147. doi:10.1016/j.jhsa.2009.04.023 [PMID:19643295].
4. Jones NF, Jupiter JB, Lalonde DH. Common fractures and dislocations of the hand. Plast Reconstr Surg.
2012;130(5):722e–736e. doi:10.1097/PRS.0b013e318267d67a [PMID:23096627].
5. Madan SS, Pai DR, Kaur A, Dixit R. Injury to ulnar collateral ligament of thumb. Orthop Surg.
2014;6(1):1–7. doi:10.1111/os.12084 [PMID:24590986].
6. Carlsen BT, Moran SL. Thumb trauma: Bennett fractures, Rolando fractures, and ulnar collateral
ligament injuries. J Hand Surg Am. 2009;34(5):945–952. doi:10.1016/j.jhsa.2009.03.017
[PMID:19411003].
7. Pellegrini Jr VD. Fractures at the base of the thumb. Hand Clin. 1988;4(1):87–102 [PMID:327798].
8. Gilula LA. Carpal injuries: analytic approach and case exercises. AJR Am J Roentgenol.
1979;133(3):503–517 [PMID:111512].
9. Suh N, Ek ET, Wolfe SW. Carpal fractures. J Hand Surg Am. 2014;39(4):785–791. quiz 791.
doi:10.1016/j.jhsa.2013.10.030 [PMID:24679911].
10. Welling RD, Jacobson JA, Jamadar DA, Chong S, Caoili EM, Jebson PJ. MDCT and radiography of
wrist fractures: radiographic sensitivity and fracture patterns. AJR Am J Roentgenol. 2008;190(1):10–16
[PMID:18094287].
11. Scalcione LR, Gimber LH, Ho AM, Johnston SS, Sheppard JE, Taljanovic MS. Spectrum of carpal
dislocations and fracture-dislocations: imaging and management. AJR Am J Roentgenol.
2014;203(3):541–550. doi:10.2214/AJR.13.11680 [PMID:25148156].
12. Gelberman RH, Cooney III WP, Szabo RM. Carpal instability. Instr Course Lect. 2001;50:123–134
[PMID:11372306].
13. Trumble TE, Culp RW, Hanel DP, Geissler WB, Berger RA. Intra-articular fractures of the distal aspect
of the radius. Instr Course Lect. 1999;48:465–480 [PMID:10098077].
14. Ruchelsman DE, Christoforou D, Jupiter JB. Fractures of the radial head and neck. J Bone Joint Surg
Am. 2013;95(5):469–478. doi:10.2106/JBJS.J.01989 [PMID:23467871].
15. Sandstrom CK, Kennedy SA, Gross JA. Acute shoulder trauma: what the surgeon wants to know.
Radiographics. 2015;35(2):475–492. doi:10.1148/rg.352140113 [PMID:25763730].
16. Simovitch R, Sanders B, Ozbaydar M, Lavery K, Warner JJ. Acromioclavicular joint injuries: diagnosis
and management. J Am Acad Orthop Surg. 2009;17(4):207–219 [PMID:19307670].
1. What is the most common direction of shoulder dislocation?

A. Anterior
B. Posterior
C. Medial
D. Lateral
2. Among the following carpal bones, which is most frequently fractured?

A. Capitate
B. Hamate
C. Lunate
D. Scaphoid
3. Which eponym is most closely associated with a fracture of the distal radial
shaft and dislocation of the distal radioulnar joint?
A. Essex-Lopresti
B. Monteggia
C. Maisonneuve
D. Galeazzi
4. Volar plate fractures of the hand are most common at which joint?
A. Distal interphalangeal joint
B. Proximal interphalangeal joint
C. Metacarpophalangeal joint
D. Carpometacarpal joint

1. A The most common shoulder dislocation is anterior.
2. D The scaphoid is the most commonly fractured carpal bone.
3. D The Galeazzi injury consists of a distal radial shaft fracture and dislocation
of the distal radioulnar joint.
4. B Volar plate fractures of the hand occur most commonly at the PIP joints.
3
Imaging of Lower Extremity
Fractures and Dislocations
Refky Nicola, Manickam Kumaravel, Stanislav Belchuk, and Felix S. Chew
Trauma is the most common reason for imaging the lower extremity.
Radiography is always the initial study performed, sometimes supplemented by
CT or MRI.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of lower extremity fractures and
dislocations, the learner will be able to
3. summarize relevant concepts and knowledge for the following anatomic regions: pelvic ring,
acetabulum and hip, proximal femur, shaft and distal femur, knee, tibia, ankle, and foot.
PELVIC RING ANATOMY

The pelvic ring comprises the sacrum and the 2 innominate bones. These 3 rigid
components have resilient articulations where small degrees of motion are
possible: the sacroiliac (SI) joints and the pubic symphysis. Thus, the pelvic ring
is not a single rigid structure. Biomechanically, the sacrum can be considered the
keystone of a femoral-sacral arch that supports the spine over the legs. The upper
portion of the SI joint is a fibrous articulation with an extremely strong
interosseous ligament; the lower portion of the SI joint is synovial and does not
contribute mechanical strength to the joint. Anterior and posterior sets of SI
ligaments attach the upper sacrum to the ilium, and sacrotuberous and
sacrospinous ligaments attach the lower sacrum to the ischium. The functional
stability of the pelvic ring depends on these ligaments. The pubic rami act as a
stabilizing strut anteriorly, but their role is not crucial, provided that the posterior
structures remain intact. Fractures of the pelvis can be divided into those that do
not disrupt the integrity of the weight-bearing femoral-sacral arch (stable
fractures) and those that do (unstable fractures).
STABLE PELVIC RING FRACTURES

Stable fractures account for approximately two-thirds of all pelvic fractures.
These injuries include isolated fractures of the sacrum and pubic rami, avulsion
fractures around the periphery of the pelvis, and simple acetabular fractures.
Many stable fractures of the pelvis, especially isolated fractures around the
obturator foramen, are sustained by elderly osteoporotic adults who fall.
Although the bony margins of the obturator foramen form a rigid ring, the
arrangement of its components is such that when the ring is loaded, one portion
may be subjected to shearing forces, whereas another may be subjected to
compressive forces. Bone resists shearing forces less well than compressive
forces, so the bones may fail under shear but not under compression, leaving a
single fracture of the ring. The most common pelvic fracture is an isolated
fracture of an ischial ramus sustained in a fall. An isolated fracture of an iliac
wing is called a Duverney fracture. It is frequently sustained in blunt trauma,
such as motor vehicle crashes.
Isolated fractures of the sacrum are caused by direct trauma or a fall. These
fractures tend to be transversely oriented, below the level of the SI joints and
anteriorly displaced or anteriorly angulated (Figures 3.1 and 3.2). They are best
demonstrated on the lateral radiograph or by sagittal CT. Fractures of the sacrum
that occur with pelvic ring fractures are typically vertical in orientation.
Stress fractures of the pubic rami may occur in runners. The clinical
presentation is groin pain that is much worse with activity. As with stress
fractures elsewhere, a radionuclide bone scan may be necessary to identify the
injury.
UNSTABLE PELVIC RING INJURIES

Unstable injuries of the pelvic ring are the result of severe trauma, usually motor
vehicle collisions involving pedestrians, operators, or passengers.1 Because these
injuries are common in the setting of multiple trauma, an anteroposterior (AP)
radiograph of the pelvis should be part of the initial evaluation of all multiple
trauma patients. Patients with pelvic fractures may have serious vascular injury,
exsanguinate, and die.2 Because reduction and stabilization of pelvic fractures
usually control bleeding, early discovery and evaluation of these injuries have
significant practical importance for the orthopedist. Urologic injuries are
commonly associated with severe pelvic fractures. Fractures that involve the
vagina or rectum are open fractures and carry a grave risk of sepsis. Three
distinct patterns of injury can be recognized (Figure 3.3).
•
FIGURE 3.1 Fracture of the sacrum. Lateral radiograph shows a transverse fracture
(arrow) through the sacrum at the S3 level.
The most common mechanism of unstable pelvic ring injury is lateral

compression. Lateral compression may occur when a pedestrian or a vehicle
occupant is struck from the side. The pelvis is crushed as the hemipelvis on the
side of impact is rotated inward by the force, sustaining a shear fracture of the
pubis and a compression fracture of the ipsilateral sacral ala; ligamentous injury
is minimal (Figure 3.4). With force of greater magnitude, continued inward
rotation causes either disruption of the posterior SI ligaments or fracture of the
ilium. The opposite hemipelvis may be rotated outward, opening that SI joint
anteriorly. Central hip dislocation may be associated with lateral pelvic
compression injuries (Figure 3.5). The severity of the injury depends on the
precise direction and magnitude of the forces.
When force is applied anteriorly to the pelvis, the pelvis is flattened open.
The anterior arch is first pulled apart and sustains a tension injury, usually a
vertically oriented tension fracture of the pubic ramus or, less often, soft tissue
disruption of the symphysis. If the force is of sufficient magnitude, one
hemipelvis rotates outward, opening the pelvis like a book (Figure 3.6). The
sacrotuberous and sacrospinous ligaments are disrupted in turn and followed by
the anterior, interosseous, and posterior SI ligaments. An even more severe
injury is total SI joint disruption that leaves a floating, unsupported hemipelvis.
AP compression fractures are associated with massive vascular damage and high
mortality rates. A posterior column acetabular fracture may be an associated
injury.
A variant of the anterior compression fracture is the straddle fracture, which
refers not to the mechanism of injury but to the morphology of the fractures. In
this situation, there are bilateral vertical fractures of the superior and inferior
pubic rami, with an intact pubis (Figure 3.7).
•
FIGURE 3.2 Fracture of the sacrum. Oblique coronal T1 MRI shows dark signal
(arrow) extending vertically along the left sacral ala, indicating the fracture line and
adjacent hemorrhage and edema.
Vertical shear forces typically occur in falls from a height onto an extended
leg. The usual pattern of injury is a vertical fracture of the anterior ring and
fracture dislocation of the ipsilateral SI joint with vertical displacement
(Malgaigne fracture) (Figure 3.8). The vertical fractures of the anterior ring may
be ipsilateral or contralateral to the SI joint lesion. Because there is total
disruption of the posterior ligaments combined with anterior fractures, this
relatively uncommon injury is grossly unstable. Occasionally, both SI joints are
dislocated as the sacrum drops through the femoral-sacral arch.
Complex patterns of pelvic ring fractures occur with the application of forces
from 2 or more directions, either together or sequentially. The most common
combination is lateral compression and AP compression. The injuries have
features of both types of injury. One helpful clue in the analysis of pelvic ring
fractures is the direction of displacement of the acetabulum. In lateral
compression injuries, the acetabulum moves medially; in AP compression, it
moves laterally; and in vertical shear, it moves superiorly. The configuration of
pubic rami fractures is another helpful clue. Pubic rami fractures oriented in the
horizontal or coronal planes are sustained under lateral compression; fractures
oriented in the vertical plane are sustained under AP compression or vertical
shear.
ACETABULAR FRACTURES
The acetabulum is nestled at the confluence of the ilium, pubis, and ischium
under an arch formed by 2 columns: the iliopubic (anterior) and ilioischial
(posterior). The posterior column, the thicker of the two, includes the major
portion of the acetabular roof. The acetabular roof, or dome, is the articular and
weight-bearing surface of the hip socket and includes portions of both columns.
The quadrilateral plate forms the medial wall of the acetabulum and does not
bear weight. The anterior column forms the iliopectineal line on AP radiographs;
the posterior column forms the ilioischial line. Each column has a wall and a
rim. Acetabular fractures result from indirect forces transmitted through the
femoral head, most often in high-energy motor vehicle collisions or falls.
Approximately 20% of pelvic ring fractures in adults involve the acetabulum.
The morphology of the fracture depends on the position of the femur at the
moment of impact, the magnitude and direction of the force, and the strength of
the bone. Acetabular fractures can be simple or complex.3 Complex fractures can
be described as combinations of fractures of the anterior and posterior columns,
the anterior and posterior rims, and the acetabular roof. A transverse fracture
separates the innominate bone into a superior iliac fragment and an inferior
ilioischial fragment, and a T-shaped fracture combines a transverse fracture with
a vertical separation of the anterior and posterior columns. The most common
fracture of the acetabulum is a simple fracture of the posterior rim (Figure 3.9),
sometimes associated with posterior hip dislocation (discussed in the next
section). The other common fractures are simple transverse fractures and
complex fractures that involve the posterior column. With complex fractures, the
orthopedist is often most concerned about whether both anterior and posterior
columns are involved or separated from each other, the severity of acetabular
dome involvement, and the concomitant presence of pelvic ring injuries,
especially ipsilateral iliac wing fractures or SI joint disruption. CT is often
necessary for full delineation of the sites of fracture and configuration of the
fragments. Acetabular fractures can also be demonstrated by 3-dimensional
reconstructions or radiographs of the pelvis in 45° oblique projections (Judet
views) that show the anterior and posterior columns (Figure 3.10). CT is often
helpful for identifying intra-articular fragments following reduction of a
fracture-dislocation of the acetabulum (Figure 3.11).
•
FIGURE 3.3 Diagram of pelvic ring fractures. A, Lateral compression (type I).
Sacroiliac (SI) joint compression and pubic ramus fracture. The hemipelvis on the
side of impact rotates inward. B, Lateral compression (type II). The SI joint is opened
posteriorly as the hemipelvis continues to rotate inward. C, Anteroposterior
compression fracture (type II). Diastasis of the symphysis with opening of the SI joint
anteriorly. D, Vertical fracture-dislocation of a hemipelvis.
•
FIGURE 3.4 Lateral compression fracture. CT shows a buckle fracture of the right
sacral ala (arrow).
•
FIGURE 3.5 Lateral compression fracture with complex acetabular fractures. A,
Anteroposterior radiograph shows fractures of the inferior pubic ramus (arrowhead),
complex fractures of the acetabulum (short arrows), fracture of the iliac wing (long
arrows), and very subtle fractures of the sacral ala, all on the right side. B, CT at the
level of the sacral ala shows a shear fracture of the iliac wing (short arrow) and
compression fracture of the sacrum (long arrow). C, CT at the level of the hips shows
fractures of both the anterior (arrow) and posterior (arrowhead) columns of the
acetabulum.
•
FIGURE 3.6 Anteroposterior compression fracture. A, There is diastasis of the
symphysis pubis (arrow). B, The left sacroiliac joint has opened anteriorly (arrow).
HIP DISLOCATION
Hip dislocations result from severe trauma such as motor vehicle collisions.
Posterior dislocations with or without acetabular fractures (Figure 3.12) account
for 85% to 90% of cases. The mechanism of posterior dislocation is a blow
along the axis of the femoral shaft with the hip flexed (as in hitting the
dashboard with the knee in a motor vehicle collision). The posterior wall or
column of the acetabulum is often fractured, and the femoral shaft or knee may
also be injured. Sciatic nerve injury, sometimes transient, is present in
approximately 10% of cases. Anterior dislocations may occur in motor vehicle
collisions or falls from heights when the hip is abducted (Figure 3.13). CT can
identify intra-articular fragments and confirm relocation of the hip after
reduction.4 The presence of a gas bubble within the hip capsule is indicative of
previous dislocation. Complications of hip dislocation include avascular necrosis
of the femoral head, transient or permanent sciatic nerve palsy, myositis
ossificans, and posttraumatic degenerative joint disease. A fragment of the
femoral head may shear off as the hip is dislocated (Figure 3.14).
•
FIGURE 3.7 Straddle fractures of the pelvis, involving the right and left superior and
inferior pubic rami (arrows).
•
FIGURE 3.8 Vertical shear fractures sustained in fall. Vertical fractures extend from
the left pubic rami through the iliac wing (arrows).
PROXIMAL FEMUR
Fractures of the proximal femur are common in the elderly.5 More than 95% of
these fractures occur in patients older than 50 years, and the incidence is
increasing as the population ages. The eventual mortality rate associated with hip
fractures approaches 20%, and many survivors lose their independence of
movement. Ninety-nine percent of fractures of the proximal femur are caused by
simple falls. Even osteoporotic femurs are resistant to the compressive and
tensile forces that occur during normal weight bearing, but there is great
vulnerability to torsional or shearing stress. The roles of preexisting
insufficiency microfractures in osteoporotic bones and decreased muscle tone as
they relate to proximal femur fractures are unclear. Patients present with a
painful, shortened, externally rotated limb that is unable to bear weight. Femoral
fractures in persons younger than 40 years result from high-energy trauma and
usually have associated injuries. Fractures of the proximal femur can be
classified as intracapsular in 37% of cases, intertrochanteric in 49%, and
subtrochanteric in 14%. Women sustain 3 to 6 times as many intracapsular
fractures as men, but the incidence of intertrochanteric fractures is equal between
the sexes. The initial evaluation in a suspected fracture should begin with
radiographs. If a fracture is not identified and there is high clinical suspicion of a
fracture, MRI should be obtained. If MRI is not available, CT or radionuclide
bone scans should be used, although they are slightly less accurate than an MRI
scan. In the elderly population, fractures may not show radionuclide uptake until
several days after the injury. A patient who was ambulatory before the fall but is
unable to bear weight afterward should be presumed to have a fracture until
proved otherwise.
•
FIGURE 3.9 Posterior wall acetabular fractures (arrow).
INTRACAPSULAR FRACTURES
The capsule of the hip joint encloses the head and most of the neck of the femur,
extending from the acetabulum to the intertrochanteric line anteriorly and to the
midneck posteriorly. Most femoral neck fractures are intracapsular and therefore
heal less rapidly (synovial fluid lyses clot) than intertrochanteric and
subtrochanteric fractures. In addition, the vascular supply to the head is largely
disrupted. Subcapital femoral neck fractures extend transversely across the neck,
just below the femoral head. Intracapsular fractures can be classified as either
nondisplaced (Figure 3.15) or displaced (Figure 3.16). Fractures through the
base of the neck are similar to 2-part intertrochanteric fractures in mechanism
and treatment (discussed in the next section). The greater the displacement, the
greater the likelihood of subsequent femoral head osteonecrosis. With displaced
fractures, the incidence of osteonecrosis and nonunion is approximately 25%.
Patients with impacted fractures are usually ambulatory with an antalgic limp
and pain that is referred to the groin or the medial knee. Nondisplaced fractures
have no inherent stability and may displace with continued ambulation. Femoral
neck fractures heal by endosteal callus formation. Nondisplaced fractures are
usually fixed with multiple pins placed in parallel; displaced fractures may be
reduced and fixed with a variety of methods, including multiple pins, a
telescoping hip screw, or some combination thereof. When the risk of femoral
head osteonecrosis is high or the quality of trabecular bone is too poor for
internal fixation, femoral endoprosthesis or total hip replacement may be used as
primary treatment.
•
FIGURE 3.10 Complex right acetabular fracture involving both columns (arrows). A
and B, Judet views reconstructed from CT.
•
FIGURE 3.11 Partially reduced posterior fracture dislocation of the right hip.
Fractures of the rim and wall of the posterior column of the acetabulum are present.
Because of the intra-articular fragment, the dislocation is not fully reducible. A fat-fluid
level and gas bubble (arrow) are present.
INTERTROCHANTERIC FRACTURES
The major fracture line of intertrochanteric fractures extends diagonally from
superolateral (greater trochanter) to inferomedial (lesser trochanter). Most
intertrochanteric fractures are comminuted, with the greater and lesser
trochanters sometimes presenting as separate fragments (Figure 3.17). In
describing these fractures, the major fragments and the fracture lines should be
enumerated in relation to the trochanters, the neck, and the shaft. The degree of
displacement and comminution and the presence or absence of subtrochanteric
extension along the femoral shaft affect the orthopedic treatment plan and
prognosis. Open reduction and internal fixation with a dynamic hip screw are
usual. Unlike intracapsular femoral neck fractures, these injuries tend to heal
promptly and without complication. The incidence of avascular necrosis of the
femoral head is approximately 1%. Incomplete intertrochanteric fractures may
occur in elderly adults as a result of falls. Radiographs in this circumstance may
be normal, but MRI will demonstrate the fracture. Isolated fractures of the
greater trochanter occur in elderly adults as a result of direct trauma sustained in
falls. Isolated fractures of the lesser trochanter in adults are pathologic and
usually indicate an underlying osseous metastasis (see chapter 12).
SUBTROCHANTERIC FRACTURES
Subtrochanteric fractures in the elderly may represent extensions of
intertrochanteric fractures into the shaft. In other age groups, subtrochanteric
fractures are sustained in high-energy trauma such as motor vehicle collisions
(Figure 3.18). The opposing pull of the gluteal and iliopsoas muscles and the
thigh adductor muscles distracts and angulates the major fracture fragments. The
cantilevered configuration of the femoral shaft and neck creates large stresses on
the medial femoral cortex that complicate orthopedic management. A possibility
of a pathologic or insufficiency fracture must be considered in subtrochanteric
fractures that occur in the absence of significant trauma.
•
FIGURE 3.12 Posterior fracture-dislocation of the right hip. A, Radiograph shows
the femoral head lateral and superior to the acetabulum. The femoral shaft is
adducted. B, CT shows the femoral head posterior to the empty acetabulum.
•
FIGURE 3.13 Anterior dislocation of the hip (different patients). A, Radiograph
shows the femoral head is inferior to the acetabulum. The femoral shaft is abducted.
B, CT shows the femoral head is anterior to the obturator ring.
SHAFT AND DISTAL FEMUR FRACTURES

Fractures of the femoral shaft occur typically in young adults as a result of major
blunt force trauma, such as motor vehicle crashes. Because the femur is the
largest and strongest bone in the human body and is protected by the largest and
strongest muscle groups, considerable force is necessary to fracture it. Blood
loss of 2 or more units typically accompanies an acute femoral shaft fracture.
When the femoral shaft fractures with minimal trauma are found in an adult, an
underlying pathologic lesion should be sought. Femoral fractures may also occur
when osteoporosis or other metabolic bone conditions are present (Figure 3.19).
Intercondylar fractures of the femur are typically the result of high-energy
trauma, such as motor vehicle crashes. Intercondylar fractures may be T-shaped
or may occur with severely comminuted distal femoral shaft fractures (Figure
3.20).
•
FIGURE 3.14 Posterior fracture-dislocation of the femoral head with a fragment
remaining in the acetabulum. A fat-fluid level and gas bubble are present in the joint.
KNEE
Radiographs are frequently obtained in the initial evaluation of knee injuries.
Radiographs may show fractures, joint effusion, and dislocation or subluxation.
Small avulsion fractures may indicate major ligamentous disruptions. Most knee
injuries involve the ligaments and other soft tissue structures (see chapter 5).
Avulsion fractures about the knee typically portend significant ligamentous
injury.6 An avulsion fracture of the medial aspect of the medial femoral
epicondyle is the result of avulsion by the medial collateral ligament and is
called a Stieda fracture. Avulsion of the tibial spines, also called the
intercondylar or median eminence, is associated with anterior cruciate ligament
injury. An avulsion fracture of the lateral margin of the proximal tibia is called a
Segond fracture (Figure 3.21). Corresponding to avulsion by the anterolateral
ligament, Segond fractures are highly associated with anterior cruciate ligament
tears. An avulsion fracture of the head of the fibula, sometimes called an arcuate
fracture (Figure 3.22), is highly associated with injuries of the posterior cruciate
ligament and of the posterolateral corner of the knee (see chapter 5). Avulsion
fractures of the medial patella suggest previous lateral patellar dislocation. When
the mechanism of injury or the clinical examination suggests ligament, cartilage,
or other soft tissue injury, MRI is the imaging method of choice for further
evaluation.
Knee dislocation involving the femorotibial joint may occur in anterior,
posterior (Figure 3.23), medial, lateral, and rotatory directions. Injury of 2 or
more ligaments is typical. Vascular and nerve injuries may be associated with
knee dislocation, so rapid reduction and vascular assessment are important. At
the University of Washington, we typically perform CT angiography.
•
FIGURE 3.15 Impacted subcapital femoral neck fracture in an elderly woman. A,
Anteroposterior radiograph shows subtle contour abnormality of the lateral cortex at
the head-neck junction (arrow) with linear density traversing the neck. B, Frog lateral
radiograph shows buckled posterior cortex (arrow).
Patellar dislocations are typically lateral dislocations and may occur with
flexion and internal rotation of the femur on a fixed tibia. They may reduce
spontaneously when the knee is extended. Impaction injuries of the medial
patella and lateral femoral condyle and tears of the medial patellofemoral
ligament characteristically accompany lateral patellar dislocations. Medial,
inferior, superior, and intracapsular dislocations of the patella are rare.
Injuries to the extensor mechanism may result from forced flexion during
strong quadriceps contraction. With complete disruption of the extensor
mechanism, voluntary knee extension is lost; a partial disruption results in
weakness of extension. In the adult, the extensor tendons are thinnest where they
pass over the patella. Tearing of the tendon coupled with a fracture of the patella
from tensile loading results in a transverse patellar fracture with the fragments
distracted by the quadriceps muscle (Figure 3.24). Patella alta refers to high
position of the patella (Figure 3.25) and may occur after rupture of the
infrapatellar tendon as the unopposed pull of the quadriceps elevates the patella.
Patella baja refers to low position of the patella, which may occur after rupture
of the quadriceps tendon. Patella baja may also accompany shortened femoral
shaft fractures where fragments are overlapping. Stellate fractures of the patella
may be caused by a direct blow. The extensor mechanism remains intact, and the
fragments are not distracted (Figure 3.26).
FIGURE 3.16 • Displaced subcapital femoral neck fracture (arrows). A,

Anteroposterior radiograph. B, True lateral radiograph.
•
FIGURE 3.17 Four-part intertrochanteric fracture with the greater and lesser
trochanters as separate fragments.
•
FIGURE 3.18 Subtrochanteric fracture in a 66-year-old man sustained in a motor
vehicle crash.
•
FIGURE 3.19 Osteoporotic supracondylar femur fracture. Lateral radiograph shows
fat-fluid level (arrow).
•
FIGURE 3.20 Intercondylar femur fracture. Anteroposterior radiograph shows
comminuted distal femur fracture with extension into the intercondylar notch,
separating the condyles.
•
FIGURE 3.21 Segond fracture of the lateral tibial margin (arrow).
TIBIAL PLATEAU
Most tibial plateau fractures are sustained in motor vehicle collisions, but
fractures of the tibial plateau may also occur in older individuals during twisting
falls (Figures 3.27–3.29). Isolated lateral tibial plateau fractures are the most
common (55%-70%); the rest involve the medial plateau alone or both plateaus.
These injuries consist of compression fractures of the subchondral cancellous
bone with depressions of the articular surface, vertical splits (shear fractures) of
the joint margin, or a combination of depression and vertical split. A knee
effusion is invariably present. CT can establish the depth of the depression and
the number and location of depressed fragments. Associated injuries include
lateral meniscal tears (50% of cases), lateral femoral condylar fractures, cruciate
ligament tears, and fibular head fractures. These injuries may be treated
surgically, depending on the amount of depression and displacement.
Posttraumatic degenerative joint disease occurs in 20% of cases. The Schatzker
classification is commonly used to describe depressed tibial plateau fractures.7
TIBIAL SHAFT
Transverse (Figure 3.30) and segmental tibial shaft fractures commonly occur in
high-energy motor vehicle collisions, particularly in pedestrians and
motorcyclists.8 Because the soft tissues covering the tibia anteriorly are thin,
many of these fractures are open. The complications of infection and
osteonecrosis of large cortical fragments are common. Even if uncomplicated,
these high-energy fractures tend to heal slowly and may take as long as 2 years
to unite completely. The combination of transverse fractures of the femoral and
tibial shafts isolates the knee joint and is called a floating knee. Twisting injuries
may result in spiral fractures of the tibia, whereas bending injuries may result in
transverse fractures with a butterfly fragment.
•
FIGURE 3.22 Fibular head avulsion fracture. A, Anteroposterior radiograph shows
avulsion fracture of the head of the fibula (arrow). B, Lateral radiograph shows a joint
effusion (short arrow). The fibular fracture is difficult to see (long arrow).
•
FIGURE 3.23 Posterior knee dislocation sustained in a motor vehicle crash.
ANKLE MORTISE
The leg articulates with the foot at the talus. The talus is a hard, slippery bone
with much of its surface covered by articular cartilage. Because the talus has no
direct muscular control, its movements follow the push and pull of adjacent
bones and ligaments. The talus is maintained in the ankle mortise (tibiofibular
socket) by geometric fit and with ligaments. The articular surfaces of the ankle
mortise are the tibial plafond superiorly and the medial (tibial) and lateral
(fibular) malleoli on either side. The mortise is wider anteriorly than posteriorly.
The posterior lip of the tibia is designated the posterior malleolus. At the distal
tibiofibular syndesmosis, anterior and posterior tibiofibular ligaments bind the
fibula to the tibia. The tibial and fibular shafts are also joined along their length
by an interosseous membrane. The lateral malleolus is attached to the foot by
anterior and posterior talofibular ligaments and a calcaneofibular ligament. The
medial malleolus has a superficial deltoid ligament that inserts on the talus,
calcaneus, and navicular and a deep deltoid ligament that inserts on the talus.
The mortise, ligaments, and calcaneus form a ring in the coronal plane with the
talus in the center (Figure 3.31). Most ankle injuries are sustained by indirect
loading when the leg angulates or rotates around a malpositioned and stationary
foot. Forced movement of the talus breaks open the mortise. Most ankle injuries
are reduced or partially reduced by the time they are radiographed, so the
direction and magnitude of loading must be inferred from the pattern of injury.
The most useful classification of ankle injuries is the AO-Weber classification
(Table 3.1). The Lauge-Hansen classification is based on biomechanical studies
of cadavers and may also be useful.9 Ankle injuries may also be described by the
location and morphology of the fractures. A practical mechanistic classification
of indirect ankle injuries has 4 types: adduction, external rotation, abduction, and
axial compression.
•
FIGURE 3.24 Avulsion fracture of inferior pole of patella (arrow).
•
FIGURE 3.25 Infrapatellar tendon sprain (grade III). Proximal retraction of the
patella by the quadriceps muscles. Note high position of patella (patella alta).
•
FIGURE 3.26 Minimally displaced comminuted patellar fracture (long arrow) from
direct trauma. Cross-table lateral radiograph demonstrates a fat-fluid level (short
arrow) indicative of intra-articular fracture.
•
FIGURE 3.27 Severely comminuted lateral tibial plateau fracture.
Adduction or inversion of the foot is inward rotation along the foot’s long
axis. With forcible inversion, the lateral malleolus and its ligaments are loaded.
The first injury is a sprain of the anterior talofibular ligament, which may be
followed by a sprain of the calcaneofibular ligament. The appearance on
radiographs is lateral soft tissue swelling; the talus may be tilted but will not be
displaced. This lateral ankle sprain is the most common ankle injury in adults
(Figure 3.32). Less commonly, a tension fracture of the lateral malleolus occurs
rather than a ligamentous sprain. With continued loading, the talus impinges
against the medial malleolus and moves medially, causing an oblique or vertical
shear fracture of the medial malleolus as the talus subluxates.
External rotation of the foot loads the anterior portion of the lateral malleolus
and the posterior portion of the medial malleolus as the talus moves within the
mortise like a lever. The first injury is disruption of the anterior tibiofibular
ligament of the syndesmosis. Loading then transfers to the lateral malleolus,
resulting in a short oblique fracture that runs anteroinferior to posterosuperior
(Figure 3.33). With continued loading, the talus displaces the lateral malleolar
fragment, causing the posterior malleolus to be avulsed by the strong posterior
tibiofibular ligaments; the lateral and posterior malleoli remain attached to the
talus and each other. Finally, with the loss of the lateral and posterior supports of
the ankle, the medial side is loaded as the talus dislocates laterally and
posteriorly and either the medial malleolus fractures or the deltoid ligament tears
(Figure 3.34). In an isolated lateral malleolar external rotation injury, the talus is
subluxated; in a trimalleolar injury, it may be completely dislocated. If the
posterior malleolar fragment includes 25% or more of the articular surface, an
associated component of axial compression can be inferred. Sometimes, CT is
necessary to establish the proportion of articular surface involvement. The most
common ankle fracture in adults is an isolated lateral malleolar fracture from
external rotation.
•
FIGURE 3.28 Depressed medial tibial plateau fracture in a 20-year-old man who
was a pedestrian struck by a car. A, Cross-table lateral radiograph shows a fat-fluid
level in the suprapatellar recess. B, Anteroposterior radiograph shows a depressed
medial tibial plateau fracture. C, Coronal CT shows the fracture involved a medial
segment of the plateau (arrow).
•
FIGURE 3.29 Lateral tibial plateau fracture (arrows). A, Radiograph. B, Axial CT.
Abduction or eversion of the foot relative to the ankle causes a tension

fracture of the medial malleolus more often than a tear of the deltoid ligament.
With continued loading in abduction, the talus impinges against the lateral
malleolus and displaces it laterally, disrupting the syndesmotic ligaments or
avulsing their bony attachments. Because the talus dislocates laterally, taking the
fibula with it, the interosseous ligament tears until the fibular shaft fractures. The
fibular fracture may occur anywhere along the shaft and typically runs
inferomedial to superolateral. A proximal fracture of the fibula may be missed
on routine radiographs of the ankle.
•
FIGURE 3.30 Transverse fractures of the tibial and fibular shafts, with posterior
displacement and lateral angulation of the distal fragment. A, Anteroposterior
radiograph. B, Lateral radiograph.
•
FIGURE 3.31 Ligaments of the ankle. Lateral aspect shows the lateral collateral
ligaments. Medial aspect shows the deltoid ligament. Coronal section shows how the
structures of the ankle joint form a ring with the talus in the center. Axial section
shows how the distal fibula is attached to the tibia by the syndesmosis.
Table 3.1 AO-WEBER CLASSIFICATION OF ANKLE FRACTURES
Type Defining Characteristic

A Lateral malleolar fracture below the level of the ankle joint space
B Oblique fracture of the lateral malleolus through the syndesmosis
C Fracture of the fibula above the syndesmosis
•
FIGURE 3.32 Lateral ankle sprain as demonstrated by soft tissue swelling (arrow)
without fracture on the anteroposterior radiograph.
Three fracture eponyms may be encountered in clinical consultation. The

Maisonneuve fracture is an abduction injury with a proximal fibular fracture and
ruptured syndesmosis (Figure 3.35). The Tillaux fracture is an abduction injury
with an avulsion fracture of the anterior tibial tubercle by the anterior tibiofibular
ligament (Figure 3.36). The Wagstaffe-Le Fort fracture is an avulsion fracture of
the anterior medial portion of the distal fibula by the anterior tibiofibular
ligament.
Ankle injuries usually require anatomic restoration of the mortise; otherwise,
excessive motion and instability lead to early degenerative joint disease. Simple
ankle sprains are treated conservatively with casting and bracing. Most heal over
a period of several weeks, but a few have chronic pain and recurrent instability.
If satisfactory restoration of the mortise is not achieved by closed means, open
reduction and internal fixation may be necessary. Medial malleolar fractures are
usually fixed by lag screws. Lateral malleolar fractures may be fixed by various
methods such as cortical plates, screws, pins, or combinations of these
appliances.
Axial compression (vertical loading) fractures (also called pilon fractures) are
sustained in falls from a height or in automobile collisions where the talus is
driven into the tibial plafond. These injuries are characterized by severe distal
tibial shaft comminution, intra-articular fractures through the tibial plafond, and
talar fractures. The typical axial compression fracture has a medial malleolar
fragment and anterior, central, and posterior tibial fragments (Figure 3.37), often
with severe comminution.
•
FIGURE 3.33 Lateral radiograph shows external rotation injury of the ankle with
oblique fibular fracture (arrow).
TALUS
Lateral osteochondral fractures of the talus may occur when forced inversion
shears the lateral edge of the talar dome against the fibula (Figure 3.38).10 The
less common medial osteochondral fracture may follow impaction of the talus
against the tibia. Clinical presentation may be nonspecific ankle pain. The terms
osteochondral defect and osteochondritis dissecans are often applied to
osteochondral fractures of the talar dome. Osteochondral defects may require CT
or MRI for demonstration. Associated osteochondral injuries of the fibula or
tibial plafond may occur.
Subtalar dislocation, simultaneous dislocation of the talonavicular and
talocalcaneal joints with the talus remaining within the ankle mortise, may occur
with ground level falls and in high-energy trauma (Figure 3.39). Most subtalar
dislocations are medial, as might occur when there is an awkward landing on an
inverted and plantar-flexed foot (basketball foot). Any misalignment of the
calcaneus relative to the talus in the setting of trauma should raise suspicion for
subtalar injury. Rarely, high-energy trauma such as motorcycle crashes may
cause extrusion of the entire or major fragments of the talus, leaving the other
bones intact and in place (Figure 3.40).
Fractures of the body or neck occur through various poorly understood
mechanisms. In more severe cases, the fracture displaces, and the subtalar joint
subluxates or dislocates (Figure 3.41). Because the vascular supply of the talus
passes from distal to proximal, osteonecrosis of the proximal fragment may
occur, suggested by the acute osteoporosis that accompanies fracture healing.
Stress fractures of the talus are unusual, but their typical location is vertically
through the neck.
A fracture of the lateral tubercle of the posterior process of the talus is called
a Shepherd fracture.
•
FIGURE 3.34 External rotation fracture-dislocation of the ankle. A and B, Lateral
and anteroposterior radiographs show displaced fractures of the medial malleolus
(long arrow), lateral malleolus (arrowheads), and posterior malleolus (short arrow),
with lateral and posterior subluxation of the talus.
•
FIGURE 3.35 A, Maisonneuve fracture (arrow) of the proximal fibula. B, Associated
abduction of the lateral malleolus and tear of the syndesmosis (arrow).
CALCANEUS
Intra-articular calcaneal fractures are caused by axial loading, as in falls where
the heel sustains the initial impact or in head-on car crashes. Such calcaneal
fractures are bilateral in 10% of cases and, because of the common mechanism
of loading, may be associated with compression or burst fractures of the
thoracolumbar spine and other fractures of the lower extremities. Although the
loading that occurs during these injuries may be rapid and massive, resulting in
gross comminution, there is a consistent pattern of injury. The calcaneus, along
with the cuboid and the fifth metatarsal, forms a weight-bearing longitudinal
arch on the lateral side of the foot that supports the talus and structures above.
With excessive axial loading, the arch consistently breaks in the center at the
tarsal sinus, where the lateral process of the talus descends like an ax. The
sustentaculum tali breaks off as a separate fragment, and the arch collapses. With
continued loading, the talus may depress the posterior calcaneal facet into the
substance of the body of the calcaneus, which in turn may explode into a
multitude of tiny fragments (joint depression type) (Figure 3.42). Alternatively,
the posterior facet and superior portion of the body may shear off horizontally as
the talus is driven downward (tongue type) (Figure 3.43). The presence of intra-
articular calcaneal fractures is usually obvious on radiographs because of
flattening of the normal bony longitudinal arch and the presence of many
fragments, but the detailed characterization necessary for surgical planning
generally requires CT.11 The soft tissues are often extensively injured in
calcaneal fractures. Occasionally, if the fractures are impacted and not displaced,
a decrease in Böhler’s angle is a helpful radiographic sign. The long-term
prognosis is poor: The sequelae of residual widening of the heel and
posttraumatic subtalar degenerative joint disease are commonplace.
•
FIGURE 3.36 Tillaux fracture shown on axial CT (arrow).
The most common of the extra-articular calcaneal fractures— those not

involving the posterior subtalar joint—is an avulsion fracture of the anterior
process. This fracture occurs where the bifurcate ligament links the calcaneus to
the cuboid and navicular. These injuries may occur with an inversion of the foot
and are easily overlooked when the ankle is examined.
Stress fractures of the calcaneus typically occur through the tuberosity. The
fracture plane is perpendicular to the stress-bearing trabeculae.
MIDFOOT
The navicular is a common site for stress fractures; these are best demonstrated
by MRI. Fractures of the body of the navicular occur with major trauma and may
involve the various articular surfaces and joints (Figure 3.44). Avulsion fractures
may be associated with ligamentous injuries of the midfoot. Fracture-dislocation
of the midfoot (Chopart fracture-dislocation) may occur through the
talonavicular and calcaneocuboid articulations during incidents such as
motorcycle crashes (Figure 3.45).
FOREFOOT
Dislocation of the forefoot (Lisfranc fracture-dislocation) may occur after a
variety of traumas, including falls, longitudinal compression with hyperflexion,
and rotary loading. In most cases, multiple metatarsals are dislocated in the same
direction (homolateral), laterally and dorsally (Figure 3.46); occasionally, the
second through fifth metatarsals are dislocated laterally, and the first metatarsal
is dislocated medially (divergent) (Figure 3.47), or only the first metatarsal is
involved. A transverse fracture through the base of the second metatarsal and
avulsion fractures of the proximal metatarsals or distal tarsals are frequently
associated with Lisfranc injuries.
•
FIGURE 3.37 A, Intra-articular axial compression fracture of the distal tibia (pilon
fracture). B, Pilon fracture shown by CT at level of distal tibia.
•
FIGURE 3.38 Osteochondral fracture of the talar dome sustained in a motor vehicle
crash. A, Anteroposterior radiograph shows fracture at the lateral corner of the talar
dome (arrow). B, Axial CT shows the anterolaterally displaced osteochondral
fragment (arrow).
FIGURE 3.39 • Comminuted talar body fracture-dislocation. The calcaneus is

dislocated distally at the posterior facet (arrows). A, Lateral radiograph. B, Sagittal CT.
Avulsion fractures at the base of the fifth metatarsal, proximal to the

metatarsal tuberosity and often involving the articulation with the cuboid, are
caused by tensile loading transmitted through the lateral cord of the plantar
aponeurosis during sudden inversion of the foot. As a tension injury, the fracture
line is oriented transversely to the direction of applied force (Figure 3.48). These
fractures commonly occur with ankle trauma and generally heal with closed
treatment. If the fracture involves the articulation between the fourth and fifth
metatarsal bases, it may be called a Jones fracture, and healing may be
problematic. An extra-articular transverse fracture of the proximal shaft (Figure
3.49) is generally a stress fracture, and healing is often problematic.
•
FIGURE 3.40 Partial open talar extrusion (arrow) shown by coronal CT.
•
FIGURE 3.41 Subtalar foot dislocation. A, Lateral radiograph shows abnormal
alignment at the talonavicular (short arrow) and posterior facet (long arrow) joints. B,
Anteroposterior radiograph shows the talus remains within the ankle mortise, but the
rest of the foot has dislocated medially as a unit. The distal articular surface (arrow) of
the talus is bare.
The distal shafts of the second and third metatarsals are common locations for
stress fractures, particularly those associated with running and marching. Stress
fractures of the metatarsals may be radiographically occult at presentation and
may require a radionuclide bone scan or MRI for demonstration. With healing,
the fractures become apparent as calcified callus becomes visible.
Dislocations of the toes are relatively uncommon except at the
metatarsophalangeal joint (Figure 3.50). Stubbed toe injuries generally load the
affected digits axially, resulting in oblique fractures of the phalangeal or
metatarsal shafts (Figure 3.51). Alternatively, comminuted T-shaped or Y-shaped
fractures at the proximal ends of the phalanges may occur. Direct trauma to the
toes from dropped objects or misadventures with wheeled or motorized
conveyances are common and may result in transverse or comminuted fractures
of the phalanges (Figure 3.52).
•
FIGURE 3.42 Calcaneal fracture (joint depression). A, Lateral radiograph shows
flattening of the calcaneus (arrow). B, Sagittal CT shows impaction of the posterior
facet (arrow) into the body of the calcaneus. C, Axial CT shows comminution of the
posterior facet (arrow). D, Böhler’s angle is normally 29° to 40°.
•
FIGURE 3.43 Comminuted intra-articular calcaneal fracture (tongue type).
•
FIGURE 3.44 Intra-articular fracture (arrow) of the body of the navicular with central
comminution and subluxation (arrowhead) of the navicular first cuneiform joint.
•
FIGURE 3.45 Chopart fracture-dislocation. A, Anteroposterior radiograph shows
medial dislocation of the talonavicular (arrowhead) and calcaneocuboid (arrow) joints.
B, Sagittal CT shows talonavicular dislocation (short arrow) with comminution and
impaction fracture of the head of the talus. The cuboid articular surface (long arrow)
does not articulate with the calcaneus on this slice.
•
FIGURE 3.46 Homolateral Lisfranc fracture-dislocation (arrow).
•
FIGURE 3.47 Divergent Lisfranc fracture-dislocation. A, Anteroposterior radiograph;
B, oblique radiograph. The second through fifth metatarsals have dislocated
superiorly and laterally as a unit, whereas the first metatarsal and medial cuneiform
have dislocated superiorly and medially. There is considerable overlap of the
dislocated bones, and fracture fragments are present at the lesser tarsometatarsal
joints.
•
FIGURE 3.48 Avulsion fracture of the fifth metatarsal base (arrow).
•
FIGURE 3.49 Extra-articular fracture of the proximal fifth metatarsal (arrow).
•
FIGURE 3.50 Dorsal dislocation of the fifth metatarsophalangeal joint (arrow).
•
FIGURE 3.51 Stubbed toe injury of the fifth toe with oblique fracture (arrow) of the
proximal phalanx.
•
FIGURE 3.52 Crush injuries of the first and second toes with transverse fractures of
the distal phalanges (arrows).
References
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1. What is the most common fracture of the ankle?

A. Oblique medial malleolar fracture
B. Oblique lateral malleolar fracture
C. Transverse medial malleolar fracture
D. Transverse lateral malleolar fracture
2. Osteonecrosis is a known complication of which injury?

A. Transverse patella fracture
B. Tibial plateau fracture
C. Intertrochanteric femur fracture
D. Talar neck fracture
3. Which injury is most closely associated with the lateral compression

mechanism of pelvic ring trauma?
A. Sacral wing fracture
B. Diastasis of the symphysis pubis
C. Open-book widening of the SI joints
D. Posterior hip dislocation
4. Intra-articular fractures of the calcaneus always involve which key structure?

A. Sustentaculum tali
B. Anterior process
C. Posterior subtalar facet
D. Calcaneocuboid joint
1. B The most common ankle fracture is an oblique fracture of the lateral
malleolus.
2. D Osteonecrosis of the talar dome may follow a displaced talar neck fracture
because the blood flows from distal to proximal.
3. A Lateral compression of the pelvis is often associated with impacted
fracture of the sacral wing on the side of the loading.
4. C By definition, intra-articular fractures of the calcaneus involve the
posterior subtalar facet.
4
Imaging of Fracture Treatment and
Healing
Felix S. Chew
This chapter describes the radiologic correlates of fracture treatment and fracture
healing.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of fracture treatment and healing, the
learner will be able to
3. summarize relevant concepts and knowledge for the following topics: fracture healing,
nonoperative fracture treatment, open reduction and internal fixation, intramedullary fixation,
external fixation, soft-tissue healing and repair, grafts and implants, complications of fracture
healing, and imaging after fracture treatment.
FRACTURE HEALING
The natural history of an uncomplicated long-bone fracture is union through the
formation of callus. This secondary fracture healing occurs in 3 stages: an
inflammatory stage, a reparative stage, and a remodeling stage (Figure 4.1). In
the inflammatory stage, days to weeks after the fracture, hematoma and
devitalization of soft tissues and bone at the fracture site provoke an acute,
intense inflammatory reaction. On radiographs, soft-tissue swelling and sharp
fracture lines are present. By 10 to 14 days after injury, the fracture lines may
have become more readily visible because of bone resorption. Acute regional
osteoporosis of the involved extremity, caused by the hyperemia that
accompanies inflammation, is usual (Figure 4.2). As the hematoma organizes
into granulation tissue capable of osteogenesis, the reparative phase begins.
External periosteal callus is formed in the subperiosteal regions adjacent to the
fracture. Fibrous tissue, cartilage, and immature bone form within the mass of
granulation tissue around the fracture. This mass, called primary or soft callus, is
fusiform in shape and bridges the fracture gap. In the proper environment of
ample blood supply and limited motion and stress, the primary callus forms
bone. Ossification in primary callus may be seen on radiographs as early as
2 weeks after injury in adults. Because external callus expands the diameter of
the bone at the site of fracture healing, often by a factor of 2 or 3, mechanical
stability (clinical union) is generally achieved within 6 to 12 weeks. Radiographs
should show abundant, well-defined callus bridging the fracture site, with
fracture lines becoming fuzzy. Bone repair continues with the formation of
intramedullary (IM) callus and woven bone. The remodeling stage of fracture
healing may take place over months to years, as woven bone is remodeled along
lines of stress (Figure 4.3). In time, there may be scant radiographic indication of
the previous fracture. In contrast, fractures of cancellous bone, particularly if
affected, tend to form internal callus rather than external callus as they heal.
Healing in a fracture that is wholly confined to cancellous trabeculae may be
evident radiographically only as increasing and then decreasing sclerosis at the
fracture site (Figure 4.4).
Injuries of the soft tissues heal through the process of localized necrosis,
inflammation, and repair. Ligament and tendon injuries heal with a bridging scar
if the ends are not too far distracted. The scar may eventually remodel along
lines of stress. Cartilage heals through a different process because of the lack of
vascularization. Localized necrosis occurs, but there is no inflammatory phase.
Superficial injuries that do not extend to the bone marrow heal by migration of
cells from the synovial fluid or from elsewhere in the cartilage. In injuries that
extend to the bone marrow, an initial blood clot is replaced by granulation tissue.
The resulting fibrous scar undergoes progressive hyalinization and
chondrification to become fibrocartilage.
CLOSED FRACTURE TREATMENT

Many fractures may be treated closed—that is, without open surgery. The
fractures and soft tissues are reduced, and the fracture is stabilized but not
completely immobilized. Muscle activity, joint motion, and load transmission
promote external callus formation. Common methods of closed fracture
treatment include plaster (Figure 4.5) or fiberglass casts (Figure 4.6) and external
braces such as walking boots. Stable fractures, when subjected to normal
stresses, maintain their reduction. Skeletal traction is commonly used for pelvic
and femur fractures as a prelude to surgery. Traction is applied by placing a pin
into the extremity distal to the fracture (Figure 4.7) and connecting a pulley and
weight. Traction can be applied to fractures of the clavicle and proximal
humerus with a figure-of-eight harness or a long-arm cast, respectively.
•
FIGURE 4.1 Fracture healing of cortical bone without fixation in an adult. A, Acute
fracture of the humeral shaft. B, At 6 weeks, calcified callus is visible and the fracture
lines are becoming obscured. C, At 12 weeks, the fracture has almost completely
healed.
•
FIGURE 4.2 Acute osteoporosis accompanying the fracture healing. Radiograph
6 weeks after injury shows subchondral bone resorption (arrow).
OPEN REDUCTION AND INTERNAL FIXATION

Open reduction and internal fixation (osteosynthesis) requires surgical exposure
of the fracture. The fracture is reduced, the soft tissues are repaired, and the
fragments are fixed with hardware. Fracture fixation hardware provides
temporary mechanical stability while the healing process occurs. The stability
that comes with internal fixation is crucial to rapid restoration of mobility and
function. Fixation devices include screws, plates, rods, pins, nails, and wires.1–5
Many fixation devices can be inserted percutaneously under fluoroscopic
guidance or through minimal incisions. A second operation is necessary to
remove many types of hardware after the fractures have been healed.
Internal fixation that holds bone fragments together rigidly promotes direct
bony union (primary fracture healing). New intracortical haversian systems drill
across the fracture site, leaving cores of new bone. Fracture callus is minimal or
absent, as the osteocytes remodel the fracture away (Figure 4.8). On radiographs,
primary fracture healing is seen as a gradual disappearance of the fracture line. A
gap between fragments or excessive motion at the fracture site interferes with the
migration of osteocytes across the fracture plane, and the fracture heals through
the formation of periosteal and endosteal callus. Secondary fracture healing
occurs more slowly in fractures with internal fixation because restriction of
motion interferes with the formation of callus.
Internal fixation devices are designed to function on the biomechanical
principles of static or dynamic interfragmentary compression, bridging, or
splintage.1–5 In static compression, a metal implant holds the fracture fragments
together under compression. In dynamic compression, the implant transforms
physiologic loading into compression at the fracture site. There is direct bony
union in both types of compression. Internal fixation bridges a fracture site when
it is secured to uninjured bone on either side of the fracture. Physiologic loads
are transferred from the bone on one side of the fracture to the bone on the other
side. If the fragments are not directly apposed and there is motion between them,
periosteal and endosteal callus fills the gaps between the bones. Length and
alignment are maintained while the bones heal. Internal fixation devices that
function as internal splints allow motion at the fracture site and promote
periosteal callus while maintaining reduction.
•
FIGURE 4.3 Remodeling humeral shaft fracture. A, 3 months after injury, the
fracture is solidly bridged by bone. B, 9 months after injury, the fracture is remodeling
and the protruding portion of the distal shaft fragment is nearly gone.
•
FIGURE 4.4 Sclerosis (arrow) indicates healing fracture in the cancellous bone of
the calcaneus.
SCREWS
Orthopedic screws are available in a variety of sizes and shapes, often for use in
specific circumstances (Figure 4.9). The parts of a screw are the head, shaft,
thread, and tip. Most types of screws have a head socketed to receive a
hexagonal shaft driver and a threaded shank. The heads have a hemispheric
undersurface that allows contact even when the screw is inclined. Screws used
for cancellous bone have a wider thread diameter relative to the core shank
diameter and a deeper thread pitch (larger distance between threads) than screws
used for cortical bone. Most screws are inserted into drill holes. These holes may
be tapped or threaded to receive a screw, or the screw may be self-tapping and
cut its own threads as it is driven into the hole. Cannulated screws are hollow in
the center (Figure 4.10). These allow the placement of screws over a guide wire,
improving the ability of the orthopedist to place screws precisely. Screws are
made of metal, commonly stainless steel or titanium alloy (Figure 4.11).
Bioabsorbable screws and other nonmetallic orthopedic implants for fracture
fixation may be difficult to recognize on radiographs but have markedly
decreased artifacts on MRI (Figure 4.12). When screws are used to secure bony
fragments to each other, they are called interfragmentary screws.
Interfragmentary screws work biomechanically by converting torque applied to
the screw into axial tension between the bone fragments. When screws are used
to secure cortical plates or other hardware to bone, they are called position
screws or neutralization screws.
•
FIGURE 4.5 Plaster cast applied to distal radius fracture.
•
FIGURE 4.6 Fiberglass cast applied to distal radius fracture.
Headless screws are used where the presence of a head may interfere with
motion or cause soft-tissue irritation. Headless screws may be inserted below the
surface of the bone, which is desirable in osteochondral fractures and intra-
articular fractures. Screws with heads may also be inserted flush with the bone
surface by countersinking or drilling a larger hole for the head to drop into as the
screw is driven.
Compression screws, also called lag screws, are threaded only at the distal
portion of the shank. This type of screw compresses 2 objects together (bone
against bone or bone against another fixation device). The object into which the
screw is threaded is pulled against the object through which the screw is passed.
Maximal compression is obtained when the screw is oriented perpendicular to
the fracture plane. A fully threaded screw fixes objects together without
compressing them because the threads force them to maintain their relative
positions. Screws that are fully threaded along their shanks may also be used in
compression if the drill hole near the head (the glide hole) is drilled to a size that
the threads pass through freely. Subsequent extraction of screws is easier if they
are fully threaded. The Acutrak screw is a headless, fully threaded, cannulated
screw with a tapered profile and a variable thread pitch (Figure 4.13). The thread
pitch is wider at one end of the screw, so that each turn of the screw compresses
fragments together because of the difference in thread pitch. These screws are
commonly used for internal fixation of intra-articular fractures of small bones
such as the scaphoid. Were it not for the cost, they could be exceedingly useful
in cabinetmaking. Dynamic hip screws (such as telescoping hip screw and
sliding hip screw) (Figure 4.14) and dynamic condylar screws with side plates
are designed for dynamic compression of fractures of the proximal and distal
femur, respectively. The screw fits into a sleeve in the side plate into which it
can slide or telescope. In an intertrochanteric hip fracture, for example, the screw
extends through the femoral neck into the head, and the side plate is fixed to the
lateral cortex of the proximal shaft. With weight bearing, the unthreaded shank
of the screw slides into the sleeve at the end of the side plate, compressing the
fracture fragments together. A smaller set screw that is threaded into the near end
of the large-diameter sliding screw can be used to apply static compression to the
fracture site at the time of surgery.
•
FIGURE 4.7 Skeletal traction. Traction device applied to the distal femur for initial
treatment of pelvic ring fractures. A, Lateral radiograph. B, Anteroposterior
radiograph.
•
FIGURE 4.8 Healing internally fixed transverse fracture of the ulna with posterior
butterfly fragment. A, Immediate postoperative film shows a cortical plate has fixed
the fragments of the transverse portion of the fracture with 1 to 2 mm distraction
(short arrow) while the oblique fractures are compressed (black arrow). B, After
7 weeks, endosteal callus bridges the transverse fracture (arrow) and the oblique
fractures have remodeled and disappeared.
•
FIGURE 4.9 Common types of orthopedic screws. A, Compression or lag screw. B,
Cannulated compression screw. C, Fully threaded screw with cancellous threads. D,
Fully threaded screws with cortical threads.
•
FIGURE 4.10 Closed reduction and percutaneous screw fixation of pelvic ring
injuries, including left sacral wing and bilateral obturator ring fractures. The screws
were placed under fluoroscopic guidance through small incisions.
•
FIGURE 4.11 Ankle fracture with internal fixation. Two cannulated lag screws (long
arrow) with cancellous threads fix the medial malleolus. The cortical plate is fixed to
the fibular shaft by 3 screws (short arrow) with cortical threads and to the lateral
malleolus by 2 cancellous screws (arrowhead).
FIGURE 4.12 • Bioabsorbable screw. Radiograph of the foot shows lucency
indicating drill hole for bioabsorbable screw fixing first and second metatarsals
(arrow).
•
FIGURE 4.13 Headless, tapered, variable thread pitch compression screw (arrow)
fixing scaphoid waist fracture.
•
FIGURE 4.14 Telescoping (dynamic) hip screw fixing an intertrochanteric fracture.
•
FIGURE 4.15 K-wire fixation. Radiograph of hand shows 2 K-wires fixing a fracture
of the proximal phalanx of the middle finger.
WIRES AND CABLES

Kirschner wires (K-wires) are used to fix cancellous bone in situations in which
a screw might also be suitable. They are introduced percutaneously, and their
purchase in bone is exclusively by friction (Figure 4.15), which makes them
easier to pull out than screws. The end of the wire is typically left protruding
from the skin so that the wires can be extracted when the fracture heals.
•
FIGURE 4.16 Biomechanical concept of tension band fixation. The band transforms
tension at the tip of the olecranon into interfragmentary compression.
•
FIGURE 4.17 Tension band fixing olecranon fracture. The tension band passes
through a hole drilled in the posterior ulnar cortex and hooks over the head of the K-
wires.
A tension band transforms tensile stress into interfragmentary compression

(Figure 4.16). Tension bands are commonly used where asymmetric muscle
tension tends to distract fragments. The tension band is usually a wire loop or
figure-of-eight that is placed across the fracture site along the line of tensile
force. When the muscle contracts, the tension band acts like a hinge to compress
the fracture fragments together. For example, a transverse fracture of the
olecranon process could be fixed by a tension band along the posterior aspect of
the triceps mechanism. With the contraction of the triceps muscles, the tension
band functions as a hinge and converts the distractive force along the posterior
aspect of the olecranon to compressive force on the opposite side (Figure 4.17).
Tension bands are also commonly used to fix transverse fractures of the patella.
Cerclage wires encircle the shaft of a bone and can be used to hold fragments to
the shaft. They are usually placed in combination with IM rods or cortical plates.
Wires are made of stainless steel and cobalt chrome alloy and are commonly in
the form of monofilament wires or metallic braided cables with multiple
filaments attached with a crimp (Figure 4.18).
Flexible fixation may be used to fix structures under tension where normal
physiologic motion would be abolished by screws or other types of rigid
fixation.6,7 Common sites for flexible fixation include the coracoclavicular
ligaments (Figure 4.19) and the ankle syndesmosis (Figure 4.20). Following
reduction, tunnels are drilled in the involved bones, and a nonmetallic cable is
passed through and secured on both ends with metal buttons. The buttons should
be positioned directly over the tunnels. The currently available nonmetallic
cables are not visualized by radiography so their integrity is assessed indirectly
by button position.
•
FIGURE 4.18 Metallic braided cable used for cerclage at the femoral shaft. The
ends of the cable are secured by a crimp (arrow) because the material cannot be
easily knotted.
PLATES
Cortical plates placed on the periosteal surface are secured to bone by position
screws and should be considered internal splints for holding together structural
defects and not load-bearing members. Compression across the fracture
components is critical to protect the plate from failure. Plates function through
the biomechanical principles of static compression, dynamic compression,
buttressing, and neutralization. Static compression can be maintained by a plate
when it is applied while the fracture site is being compressed during surgery
(Figure 4.21). Compression can also be applied through specially designed screw
holes and eccentrically placed screws. Locking plates are cortical plates in which
some of the screw holes are designed to constrain the position of the screw that
is fitted to it, preventing it from toggling and fixing the relative positions of the
plate and fracture fragment (Figure 4.22). Small plates may be used to fix small
fragments. When placed on a bone with asymmetric muscle pull such as the
femur, a plate placed with initial static compression may subsequently function
with dynamic compression through the tension band principle when weight
bearing resumes. Plates can also be contoured to fit the particular shape of the
bone to which they are applied, either at the time of manufacture or at the time
of surgery. Buttress plates are broader on one end than the other and may be used
to fix metaphyseal fractures of long bones such as the distal radius or the
proximal tibia (Figure 4.23). A buttress plate used dynamically transforms
shearing stress directed along the longitudinal axis of the bone into compressive
force across the fracture plane. Neutralization plates counter the stresses on an
internally fixed fracture but are not intended to provide interfragmentary
compression. When neutralization plates are used to maintain length and
position, 1 or more interfragmentary screws may also be used to hold the
fracture fragments together. The interfragmentary screws are generally oriented
perpendicular to the fracture plane for maximum compression. Interfragmentary
screws may also pass through one of the holes in the neutralization plate.
•
FIGURE 4.19 Flexible fixation for acromioclavicular (AC) separation (type III). A,
The AC joint has been reduced and the distal clavicular shaft fixed to the coracoid
process. B, Nonmetallic cable has been threaded through tunnels and secured by
buttons.
•
FIGURE 4.20 Flexible fixation for Weber C ankle fracture. Following reduction of the
ankle and distal tibiofibular joint, the fibula was fixed to the tibia with 2 nonmetallic
cables.
•
FIGURE 4.21 Dynamic compression plate (arrow) fixing fractures of the distal radial
shaft. Note the eccentric screw placement in the oval holes of the plate. Malleable
plates have been used to fix fractures of the ulnar shaft.
•
FIGURE 4.22 Locked T-shaped plate fixing distal radius fractures with locking
screws (arrow) distally and nonlocking screws proximally.
•
FIGURE 4.23 Buttress plate fixing lateral tibial plateau fracture.
Recent developments in plate technology have emphasized low-profile

designs for specific anatomic sites and specific types of fractures.5–7 An example
is at the distal radius, a common site of fracture, where cortical plates have
become much smaller and specific plates are available for various subtypes of
fractures (Figure 4.24). Cortical plates can be used for bridging a comminuted
distal radius fracture (Figure 4.25). In this circumstance, the bridge extends from
the radial shaft, across the fracture site and the carpal bones, to the second or
third metacarpal shaft.
•
FIGURE 4.24 Specialized cortical plates for distal radius fixation. A, Small cortical
plates and screws fixing a comminuted intra-articular fracture. B, Contoured low-
profile cortical plate fixing a comminuted intra-articular fracture. The unused small
distal holes are designed for locking screws.
•
FIGURE 4.25 Cortical plate used as a bridge for comminuted intra-articular
fractures of the distal radius and ulna.
A blade plate is a cortical plate with an angled blade that is inserted sideways
into the end of a bone while the plate is affixed to the cortex of the shaft with
position screws. Blade plates are used at sites such as the proximal femur, the
distal femur, and the proximal humerus (Figure 4.26), where normal muscle pull
would tend to destabilize a simple plate. Blade plates have been replaced in
many circumstances by telescoping screws with side plates and by specialized
IM rods.
•
FIGURE 4.26 Blade plate traversing a comminuted proximal humerus fracture.
INTRAMEDULLARY RODS
IM rods or nails are used to treat long-bone fractures. In closed nailing, the rod is
inserted into one end of the fractured bone and passed across the fracture site
under fluoroscopic guidance. In open nailing, the rod is passed across the
fracture site under direct surgical visualization. The medullary space is usually
reamed so that it can accommodate the rod, destroying the endosteal blood
supply but depositing finely morselized bone and marrow elements at the
fracture site; this osseous autograft enhances fracture healing. The endosteal
blood supply reconstitutes in approximately 3 weeks. The periosteal blood
supply is preserved. An IM rod typically functions as a load-sharing device or an
internal splint. Small, flexible IM rods can be placed into small non–weight-
bearing bones. Larger bones require larger, more rigid IM rods for fixation and
strength. If the rod is locked on both ends by cross-screws (Figure 4.27), it
ceases to function as a load-sharing device and becomes a load-bearing device.
When the limb is loaded, the stresses are transferred from the bone to one end of
the rod by the cross-screws, travel along the length of the rod past the fracture
site, and finally are dispersed by the cross-screws at the other end, thus
preventing load on the fracture site. Locking also allows control and reduction of
rotary displacement. As periosteal callus is formed and the fracture begins to
stabilize, one set of locking screws may be removed, allowing load sharing by
the healing bone. This technique of removing the locking screws from the longer
fragment is called dynamization. Rods may be inserted across a fracture site in
an antegrade fashion or a retrograde fashion. The direction of insertion can be
identified on radiographs by the locations of the blunt and tapered ends, with the
tapered end pointing in the direction of insertion and the blunt end located at the
site of insertion. New designs in IM rods have resulted in rods intended for
fractures of specific bones, including the clavicle, humerus, radius, ulna, femur,
and tibia. These rods take into account the biomechanical requirements of each
site as well as the unique anatomy and surgical issues. For example, the gamma
nail is designed specifically for subtrochanteric femur fractures (Figure 4.28).
•
FIGURE 4.27 Antegrade intramedullary rod fixing a femoral shaft fracture. A,
Proximal locking screws (arrows). B, Distal locking screws (arrows).
EXTERNAL FIXATION
External fixation allows a fractured limb to be reduced or stabilized by the
manipulation of externally projecting pins or wires secured to the limb on both
sides of the fracture site. Surgical trauma to the fracture site is avoided. The
fixation is more rigid and allows earlier mobility than closed methods. The
fractures unite by secondary bone healing. External fixation is favored for types
II and III open fractures, in which distraction of the limb is appropriate and rapid
surgical stabilization is necessary. The 2 major types of external fixators are pins
attached to rods (pin fixators) and wires stretched on circular frames that are
attached to rods (ring fixators). Pin fixators are secured to bone with pins that are
introduced surgically or percutaneously (Figure 4.29). Different fixator
configurations can be tailored to the specific fracture site and morphology. Many
fractures require external fixation in 2 planes for stability. Pin fixators can be
applied rapidly in emergent situations and are used often for pelvic fractures in
which early reduction and fixation can realign the soft tissues and avert life-
threatening hemorrhage. Ring fixators (Ilizarov fixators) are secured to bone
through a pair of crossed, unthreaded, transfixion wires that are stretched on a
circular frame.8 These circular frames are attached to longitudinal connecting
rods. The fragments are reduced by adjusting the position of the rings relative to
each other. A nonunion may be addressed by compression to induce healing
followed by distraction to restore length (Figure 4.30). A fragment of bone can
be transported axially by successive adjustments of the rings along the
longitudinal rods on the order of 1 mm/d (Figure 4.31). Modular systems of
external fixation allow the surgeon to fit hybrid frames to complex, complicated
fractures using both pins and rings.
•
FIGURE 4.28 Gamma nail fixation of a subtrochanteric femur fracture.
•
FIGURE 4.29 Comminuted intra-articular fractures of the distal radius and ulna. The
distal radius fragments have been fixed by K-wires. The entire wrist has been
stabilized by a pin-rod external fixator.
SOFT-TISSUE HEALING AND REPAIR

Tendon and ligament healing occurs in phases. Initially, the wound fills with
blood, inflammatory products, and fibrin. Proliferating granulation tissue then
fills the gap, and over a period of weeks to months, fibroblasts and collagen
fibers begin to unite the injured ends. The healing tissue then remodels and
matures, as the fibroblasts and collagen fibers become oriented along the lines of
stress, a process that may continue over many months. Direct repair of tendons
and ligaments is generally performed by suturing the injured ends together.
When a soft-tissue structure has been avulsed from a bony attachment, it may be
reattached using a variety of devices, including sutures, wires, screws, pins, and
soft-tissue anchors. When screws are used, washers are generally placed between
the screw head and the soft tissues to increase the surface area contacting the
bone and to decrease trauma caused by the screw itself. Soft-tissue anchors are
small devices that are embedded into the bone and have loops through which
sutures may be passed (Figure 4.32). Soft-tissue anchors are available in a
variety of sizes, shapes, and materials, including plastic, metal, and
bioabsorbable materials. With healing, the biomechanical integrity of the soft-
tissue attachment is reestablished.
•
FIGURE 4.30 Ilizarov external fixator for treatment of nonunion (arrow).
GRAFTS AND IMPLANTS

Soft-tissue grafts and bone grafts are commonly used to reconstruct severe open
fractures, particularly where significant fragments of bone have been ejected
from the limb at the time of trauma or debrided at the time of initial treatment
(Figure 4.33). Bone grafts used for trauma reconstruction are more commonly
small pieces of corticocancellous bone rather than massive allografts. Large
defects in cortical bone are generally reconstructed by bone transport rather than
grafting. Structural biomaterials as substitutes for bone is an active area of
research in orthopedics. Materials gaining widespread use in the United States
include genetically engineered bone growth factors, bioabsorbable hardware, and
metallic implants with bonelike mechanical and physical properties.9
FAILURE OF FRACTURE HEALING

Fracture healing is impaired or slow when the patient is elderly or in poor
nutritional condition, when the local blood supply is poor, and when the
fragments are displaced rather than apposed. Intracapsular fractures (within the
joint capsule) heal slowly because the intracapsular part of the bone does not
support periosteal callus formation, and synovial fluid lyses the blood clot.
Necrotic bone fragments cannot participate in the healing process until they are
revascularized. An extensive fracture heals more slowly than a limited one. A
fracture through cortical bone heals more slowly than one through cancellous
bone. A fracture with significant soft-tissue damage heals more slowly than one
with little soft-tissue damage. An infected fracture will not heal.
•
FIGURE 4.31 Hybrid pin-rod and ring external fixation for bone transport following
the loss of a segment of bone during an open tibial fracture. A, Lateral radiograph 1
month following trauma shows the large distal gap (arrowheads) in the tibial shaft, a
proximal tibial osteotomy (arrow), and a bone fragment (F) attached to the pin-rod
appliance. B, Lateral radiograph at 6 months shows distal transport of the fragment
(F), narrowing the distal gap (arrowheads) in the tibial shaft while the proximal tibial
shaft osteotomy (arrow) gap widens and fills with callus.
•
FIGURE 4.32 Soft-tissue anchors in the distal humerus (arrow).
Distraction of fragments or excessive motion between them may result in

nonunion. Nonunion is an arrest of the healing process before there is bony
union of the fragments. The bone ends become osteoporotic and atrophied or
hypertrophic and sclerotic (Figure 4.34; see also Figure 4.30). The space
between the bony fragments usually contains dense fibrous tissue and sometimes
may be clinically stable. Alternatively, a false joint lined with synovium and
filled with synovial fluid (pseudoarthrosis) may form in the gap between
ununited fracture fragments; this tends to occur when there has been excessive
motion at the fracture site. Malunion occurs when the fracture fragments heal in
poor position or alignment so that functional or cosmetic problems ensue. The
presence of malunion is a clinical, not a radiologic, diagnosis. Delayed union is
the situation in which there is a longer-than-average healing process, and slow
union is the situation in which the healing process is protracted but progressive.
•
FIGURE 4.33 Bone graft (arrows) for open fracture of the ankle.
Failure of an internally fixed fracture to heal is usually caused by a gap

between fragments or excessive motion at the fracture site. The result is failure
or loosening of the fixation device. Loosening is evident on radiographs by the
presence of a lucent zone around the device. This lucent zone corresponds to
resorption of bone, indicating that the device no longer has a stable purchase
(Figure 4.35). There is often a thin zone of sclerosis at the metal-bone interface
(Figure 4.36). Hardware that shifts in position from examination to examination
indicates loosening (Figure 4.37). Catastrophic loss of fixation with breakage of
hardware may occur when there is too much biomechanical stress on the
reconstructed part and there is progressive angulation or displacement (Figure
4.38).
COMPLICATIONS
Complications of fractures may be immediate or delayed (Table 4.1).
Fat embolism is an acute complication that may occur when a fracture allows
fatty marrow to gain access to the venous system. Fat is liquid at body
temperature and pours out of a fractured bone into the soft tissues, where it may
enter the veins and travel to the lungs. Fat emboli appear to provoke a chemical
pneumonitis rather than causing pulmonary infarction.
FIGURE 4.34 • Humeral shaft fracture with atrophic nonunion (arrow) and
intramedullary rod. The ends of the fragments have developed cortex.
•
FIGURE 4.35 Loose plates and screws with fracture nonunions of the radius and
ulna.
FIGURE 4.36 • Loose screws transfixing the syndesmosis for total ankle
replacement. A thin zone of sclerosis (arrows) demarcates the region of bone
resorption around the hardware.
•
FIGURE 4.37 Loose screw (arrow) protruding into soft tissues.
•
FIGURE 4.38 Fractured plate at a comminuted distal radius fracture. A, Lateral
radiograph 6 weeks after internal fixation shows mild dorsal angulation and bending of
the volar cortical plate. B, Lateral radiograph 12 weeks after internal fixation shows
progression of angulation with fracture of plate (arrow).
Table 4.1 FRACTURE COMPLICATIONS
Immediate Complications
Shock
Hemorrhage
Thromboembolism
Disseminated intravascular coagulopathy
Fat embolism
Gas gangrene
Tetanus
Osteonecrosis
Posttraumatic reflex sympathetic dystrophy
Compartment syndrome
Osteomyelitis
Delayed Complications
Posttraumatic degenerative joint disease
Posttraumatic chondrolysis
Remote stress injuries
Refracture
Chronic pain and instability
Myositis ossificans
Failure or migration of implant
Synostosis
Avascular necrosis of bone may occur when the blood supply is compromised
by the injury or by the fixation device. Normally, bones become osteoporotic in
response to fracture healing. Avascular necrosis can be recognized on
radiographs because necrotic, devascularized bone does not become osteoporotic
(Figure 4.39). Common sites of avascular necrosis after fracture include the
femoral head, the proximal pole of the scaphoid, and the proximal pole of the
talus. MRI may show osteonecrosis before radiographs.
Infection may occur as a complication of the primary injury or secondarily
during treatment. Infection can be recognized radiographically as a nonhealing
fracture with progressive bone loss, but the process may be far advanced before
radiographic changes are noticeable (Figure 4.40). External fixators are
vulnerable to infection at the insertion sites of wires or pins through the skin into
the bone (Figure 4.41). Pin infections can be recognized by osteolysis at the site
of insertion. Treatment of infected or potentially infected fractures typically
includes debridement (the removal of contaminated or devitalized tissue) and
antibiotic therapy. Antibiotic-impregnated beads may be placed directly into the
site of infection (Figure 4.42) and removed after the infection has resolved.
Untreated or unrecognized soft-tissue injuries may result in instability,
chronic pain, and devastating disability, particularly in the wrist, shoulder, knee,
and ankle. MRI may be helpful for delineating injuries to ligaments, tendons,
and cartilage in these regions.
Posttraumatic complex regional pain syndrome (such as reflex sympathetic
dystrophy and Sudeck atrophy) is a painful swelling of an extremity with rapid
onset after an injury.10 The injury may be a fracture but is often minor. The site
of swelling and pain is usually in the ipsilateral limb but remote from the site of
trauma. The cause is thought to be neurovascular. Regional soft-tissue swelling
and acute osteoporosis are evident at onset (Figure 4.43). Soft-tissue atrophy
may follow subsidence of the acute symptoms; the bone usually remains
osteoporotic.
Scars in bone may remain after the removal of internal fixation devices. Small
holes in the cortex from the removal of screws or pins do not fill in with bone
but remodel by cortication of the edges (Figure 4.44). During loading, stress
tends to concentrate at irregularities in bone or at the sites of hardware.
Subsequent fractures tend to begin at such “stress risers” (Figure 4.45).
Altered stresses and biomechanics related to a fracture may result in remote
complications such as stress injuries to contralateral limbs. A fracture with
mechanical fixation in place may not remodel because the site is shielded from
mechanical stress. An insufficiency fracture may follow the removal of the
fixation device.
Posttraumatic degenerative joint disease may occur because of direct damage
to the articular surfaces or the subchondral bone. Malunion and altered patterns
of stress on joints adjacent to a fracture site may also lead to degenerative
changes, particularly in weight-bearing joints. Posttraumatic chondrolysis is an
articular complication in which there is rapid, generalized dissolution of the
articular cartilage of the traumatized bones; the process is poorly understood.
Myositis ossificans is heterotopic ossification in the soft tissues.
Posttraumatic heterotopic ossification may follow soft-tissue injury, resulting in
mature bone formation at the site (Figure 4.46). Although mechanical problems
may ensue, the heterotopic bone will usually remodel and may ultimately be
resorbed. Occasionally, myositis ossificans may be mistaken for sarcoma on
MRI or other imaging, but clinical correlation and follow-up will clarify the
issue.
•
FIGURE 4.39 Talar neck fracture osteonecrosis. The talar dome is relatively denser
than the surrounding bones, which have regional osteoporosis related to fracture
healing.
•
FIGURE 4.40 Infected intramedullary rod. A, Radiograph of the tibia shows
lucencies (arrow) around the distal end of the rod. B, White cell scan shows intense
accumulation of activity (arrow) around the distal end of the rod.
•
FIGURE 4.41 Infected pin-rod external fixator. Focal osteolysis (arrows) is present
where the pins traverse the tibial cortex.
•
FIGURE 4.42 Antibiotic beads (arrow) at the site of an internally fixed open fracture.
•
FIGURE 4.43 Posttraumatic reflex sympathetic dystrophy. Acute osteoporosis and
painful soft-tissue swelling of the entire hand 3 months after a fracture of the
ipsilateral scapula.
FIGURE 4.44 • Healed tracts in the proximal tibial shaft where a locked
intramedullary rod was used for fixation. The margins have become corticated.
•
FIGURE 4.45 Tibial fracture line passes through screws from previous osteotomy.
IMAGING AFTER TREATMENT

Radiographs are the usual method of imaging fracture healing. Early radiographs
may be obtained to check the accuracy of the reduction and the appropriateness
of fixation device placement. Subsequent exams follow the healing process or
investigate possible complications. The presence of hardware often requires
nonstandard oblique views so that the fracture site is not obscured by the device.
Sometimes, positioning under fluoroscopy may be helpful in projecting the
metal away from the bone, revealing the fracture site. Stress radiographs may
identify motion at a fracture site, indicating nonunion (Figure 4.47). Additional
constraints on positioning for radiographs may be imposed by orthopedic
devices.
CT is excellent for demonstrating complex fractures or for identifying small
fragments; however, artifacts from metal implants may reduce image quality.
Fracture hardware and small implants such as metallic sutures or vascular clips
may produce major artifacts on MRI that limit its usefulness after fractures.
Even when nothing has been implanted, microscopic metal debris from drills and
other instruments may still produce artifacts that reduce image quality. However,
orthopedic hardware used for fracture fixation does not deflect in the magnetic
fields used for MRI, and the patients may be safely scanned. Radionuclide bone
scans are occasionally helpful in demonstrating the presence of physiologic
activity at a fracture site. Nuclear scans with labeled leukocytes or gallium as
well as FDG-PET/CT may occasionally be helpful when there is a question of
infection.
•
FIGURE 4.46 Posttraumatic heterotopic ossification.
•
FIGURE 4.47 Motion at fracture nonunion (arrow) demonstrated by anteroposterior
radiograph with stress.
References
1. Chew FS, Pappas CN. Fracture fixation hardware in the extremities. Radiol Clin North Am.
1995;33:375–390.
2. Siegel J, Tornetta III P, Borrelli Jr J, Kregor P, Ricci WM. Locked and minimally invasive plating. Instr
Course Lect. 2007;56:353–368.
3. Taljanovic MS, Hunter TB, Miller MD, et al. Gallery of medical devices: part 1: orthopedic devices for
the extremities and pelvis. RadioGraphics. 2005;25:859–870.
4. Taljanovic MS, Jones MD, Ruth JT, et al. Fracture fixation. RadioGraphics. 2003;23:1569–1590.
5. Tejwani NC, Wolinsky P. The changing face of orthopaedic trauma: locked plating and minimally
invasive techniques. Instr Course Lect. 2008;57:3–9.
6. Petscavage JM, Ha AS, Khorashadi L, Perrich K, Chew FS. New and improved orthopedic hardware for
the 21st century: part 1, upper extremity. AJR Am J Roentgenol. 2011;197(3):W423–W433.
doi:10.2214/AJR.10.5347 [PMID:21862769].
the 21st century: part 2, lower extremity and axial skeleton. AJR Am J Roentgenol. 2011;197(3):W434–
W444. doi:10.2214/AJR.10.5354 [PMID:21862770].
8. Watson MA, Mathias KJ, Maffulli N. External ring fixators: an overview. Proc Inst Mech Eng.
2000;214:459–470.
9. Tsiridis E, Upadhyay N, Giannoudis P. Molecular aspects of fracture healing: which are the important
molecules? Injury. 2007;38 (suppl 1):S11–S25.
10. Koman LA, Smith BP, Ekman EF, Smith TL. Complex regional pain syndrome. Instr Course Lect.
2005;54:11–20.
1. Secondary fracture healing is most closely associated with which mode of

treatment?
A. Cortical plate and screws
B. Interfragmentary compression screws
C. Buttress plate and screws
D. Plaster cast
2. Calcified callus at a fracture site seen at 6 to 12 weeks after trauma is most

closely associated with which condition?
A. Infection
B. Nonunion
C. Healing
D. Osteonecrosis
3. Primary fracture healing is most closely associated with which mode of

treatment?
A. Plate and screws
B. Locked IM rod
C. External fixator
D. Fiberglass cast
4. Which situation typically requires surgical intervention for fracture healing to

occur?
A. Malunion
B. Nonunion
C. Slow union
D. Delayed union

1. D Secondary fracture healing, with formation of fracture callus, occurs when
the fracture is not rigidly fixed.
2. C Calcified callus is normally present at 6 to 12 weeks in uncomplicated
secondary fracture healing.
3. A Primary fracture healing occurs with rigid fixation.
4. B Nonunion requires surgical intervention for fracture healing to resume.
5
MRI of Knee Injuries
Felix S. Chew and Kimia Khalatbari Kani
Knee pain is a common complaint in athletes and nonathletes at all levels and
ages and in all activities. Because most knee injuries involve cartilage,
ligaments, or tendons, MRI is appropriate for these patients. Initial knee
radiographs can identify fractures and other bone abnormalities and should be
the first imaging study to be performed.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of MRI of knee injuries, the learner will be able to
1. discuss and recommend appropriate MRI protocols,
2. describe relevant radiologic anatomy,
4. summarize relevant concepts and knowledge for the following topics: meniscal tears, ligament
injury biomechanics, anterior cruciate ligament (ACL) injury, posterior cruciate ligament (PCL)
injury, medial collateral ligament (MCL) injury, posterolateral corner injury, posteromedial corner
injury, multiligament injury, extensor mechanism injury, lateral patellar dislocation, bone bruise
patterns, articular cartilage injury, myotendinous injury, and miscellaneous knee syndromes.
MRI PROTOCOL
Our department has a variety of 1.5 and 3.0 T MRI scanners operated by a
diverse and changing group of technologists, so we keep our imaging protocols
relatively generic and simple. For routine knee MRI, one should generally have
imaging in the sagittal, coronal, and axial planes combined with fluid-sensitive
fat-suppressed and non–fat-suppressed pulse sequences. The exact anatomic
plane-pulse sequence combinations do not matter much. Sometimes we add an
additional plane or pulse sequence for a specific purpose. We do not use
intravenous or intra-articular gadolinium for routine knee MRI. The usual field
of view will include the suprapatellar recess at the superior extent and the
proximal tibiofibular joint at the distal extent.
DICTATION CHECKLIST
Our dictation checklist for knee MRI includes the medial and lateral meniscus,
ACL and PCL, MCL and lateral collateral complex (iliotibial [IT] band, lateral
collateral ligament [LCL], biceps femoris tendon), extensor mechanism,
posterolateral and posteromedial corners, synovium and joint capsule, bone
marrow, muscles, articular cartilage, focal lesions, cysts and masses, and
subcutaneous tissues. Each of these structures should be identified and evaluated
for morphology and signal characteristics. Any region of high signal on fluid-
sensitive sequences should attract further scrutiny. The clinical indication should
be specifically addressed.
ANATOMY
The knee joint comprises the articulation of the distal femur, patella, proximal
tibia, proximal fibula, and their supporting soft-tissue structures (Figures 5.1–
5.4). On sagittal MRI, the posterior aspect of the lateral femoral condyle should
be aligned with the posterior aspect of the lateral tibial plateau, and the posterior
aspect of the medial femoral condyle should be aligned with the posterior aspect
of the medial tibial plateau. To provide stability throughout its range of motion,
there are many static and dynamic stabilizing structures about the knee. Static
stabilizers such as ligaments are active only in certain positions and against
tensile stress; dynamic stabilizers such as muscle tendon units actively adjust to
different positions and directions of stress.
The MCL extends from the medial aspect of the femoral metaphysis to the
proximal tibial shaft (Figure 5.1A). The LCL complex consists of the IT band
that inserts along the anterolateral surface of the lateral tibial condyle, the LCL
(fibular collateral ligament) that extends from the lateral aspect of the lateral
femoral condyle to the fibular head, and the biceps femoris tendon that inserts on
the proximal fibula and proximal tibia (Figure 5.1B).
The cruciate ligaments occupy the intercondylar notch of the femur, with the
ACL lateral to the PCL. The ACL originates at the medial side of the lateral
condyle and extends anteriorly in anteromedial and posterolateral bundles to
insert anterior to the tibial spines. The PCL originates at the lateral side of the
medial condyle and extends posteriorly in posteromedial and anterolateral
bundles to the posterior aspect of the tibia. On MRI with the knee extended, the
ACL should be straight (Figure 5.2A), whereas the PCL should be relaxed and
smoothly curved (Figure 5.2B). The cruciate ligaments are within the knee
capsule (intracapsular) but outside of the synovial envelope (extrasynovial);
therefore, they should not be directly contacted by joint fluid.
•
FIGURE 5.1 Normal knee coronal T1 MRI anatomy. A, Coronal T1 MRI through the
middle of the knee showing the following structures: bodies of medial (MM) and lateral
(LM) menisci, anterior (ACL) and posterior (PCL) cruciate ligaments, medial collateral
ligament (MCL), iliotibial band (IT), vastus medialis (VM), vastus lateralis (VL), tibialis
anterior (TA), and tibial and femoral articular cartilage. B, Coronal T1 MRI through the
posterior knee showing the following structures: biceps femoris (BF), lateral collateral
ligament (LCL), proximal tibiofibular joint (TF), lateral (LH) and medial (MH) heads of
the gastrocnemius, LM and MM, and PCL.
•
FIGURE 5.2 Normal cruciate ligaments. A, Sagittal PD MRI through the lateral
portion of the intercondylar notch showing the following structures: anterior cruciate
ligament (ACL), quadriceps (QT) and infrapatellar (PT) tendons, anterior tibial
tubercle (TT), suprapatellar recess (SR) without effusion, popliteal artery (PA), and
patellar and trochlear articular cartilage. B, Sagittal PD MRI through the medial
portion of the intercondylar notch showing the following structures: posterior cruciate
ligament (PCL), popliteus muscle belly (P), Hoffa fat pad (HF), quadriceps fat pad
(QF), prefemoral fat pad (PF).
The medial and lateral menisci are 2 crescent-shaped structures that sit on top
of the tibial plateaus and deepen the articular surfaces for the femoral condyles
(Figure 5.3). The menisci are composed of fibrocartilage and have a triangular
cross section, contoured to match the shapes of the tibial plateaus and femoral
condyles. Each meniscus has 3 regions: the anterior horn, the body, and the
posterior horn, but there are no anatomic separations between these regions. The
lateral meniscus is smaller and has approximately the same cross section
throughout. The medial meniscus (MM) is larger and has a smaller anterior horn
and body and a larger posterior horn.
•
FIGURE 5.3 Normal sagittal PD FS MRI of knee anatomy. A, Lateral compartment
showing the following structures: lateral femoral condyle (LFC), lateral tibial plateau
(LTP), fibular head (FH), lateral meniscus (LM) with bow tie appearance, popliteus
hiatus (PH) with the popliteus (P) tendon passing through, and joint fluid (F) in the
lateral recess of the joint capsule. B, More central image shows anterior (AL) and
posterior (PL) horns of the lateral meniscus and the popliteus (P) tendon. C, Medial
compartment shows the medial femoral condyle (MFC) and the medial meniscus
(MM) with bow tie appearance. D, More central image shows the anterior (AM) and
posterior (PM) horns of the MM and the medial tibial plateau (MTP).
The menisci have a microarchitecture of collagen bundles with intervening

proteoglycan ground substance and cells. The peripheral portions are more
fibrous, with a circumferential arrangement of collagen bundles that maintains
the shape of the meniscus under compressive loading between the femur and
tibia, converting the compressive stress into hoop strain (circumferential
elongation). Thinner radial fibers oriented perpendicular to the circumferential
bundles tie them together to form a structural lattice. The inner portions of the
menisci are less fibrous and more like articular cartilage.
The menisci are attached centrally to the proximal tibia via the anterior and
posterior central root ligaments, the last few millimeters of meniscal tissue that
angle down to the intercondylar notch attachment sites (Figure 5.5). The menisci
are attached peripherally to the tibia by the meniscotibial ligaments (coronary
ligaments) and to the knee joint capsule. The body of the MM attaches to the
MCL. The popliteus hiatus for the popliteus tendon runs along the posterior
aspect of the lateral meniscus. There are 2 variably present posterior
meniscofemoral ligaments that may arise from the lateral meniscus and course
obliquely to attach at the medial femoral condyle. The ligament of Wrisberg
passes posterior to the PCL (Figure 5.6), and the ligament of Humphrey passes
anterior to the PCL. The menisci move with knee flexion and extension, with the
lateral meniscus being more mobile than the medial. The normal menisci are
dark on all MRI sequences (Figure 5.3) but may have high or intermediate
intrameniscal signal in the periphery in younger patients.
Intermeniscal ligaments that connect the medial and lateral menisci to each
other are variably present (Figure 5.7). The anterior (also called transverse)
intermeniscal ligament connects the anterior horns of the menisci together
(Figure 5.8) and may sometimes be mistaken for a tear of the anterior horn. The
posterior intermeniscal ligament connects the posterior horns of the menisci. The
oblique meniscomeniscal ligaments course through the intercondylar notch
between the cruciate ligaments to connect an anterior horn to a posterior horn.
The transverse intermeniscal ligament is present in approximately 90% of knees,
whereas the other variants are present in fewer than 5% of knees.
The extensor mechanism includes the quadriceps muscles and tendons, the
patella, and the infrapatellar tendon, along with the medial and lateral
patellofemoral ligaments and retinacula (Figure 5.2). The patellofemoral
ligaments and retinacula extend posteriorly from the patella and tendons to
merge with the joint capsular structures (Figure 5.4). The medial and lateral
patellofemoral ligaments are the primary static stabilizers of the patella, helping
it maintain its position and restraining it from lateral or medial subluxation,
respectively. The patella is a sesamoid bone, and the quadriceps tendon courses
over it and continues as the infrapatellar tendon, inserting at the anterior tibial
tubercle.
•
FIGURE 5.4 Normal axial T2 FS MRI of knee anatomy. A, At the level of the patella,
the quadriceps tendon (QT) passes over the anterior portion of the patella. The
medial patellofemoral ligament (MPFL) and the lateral patellofemoral ligament (LPFL)
are visible. LFC, lateral femoral condyle; MFC, medial femoral condyle. B, Axial MRI
through femoral condyles shows the posterior cruciate ligament (PCL) and anterior
cruciate ligament (ACL) within the intercondylar notch. BF, biceps femoris tendon; HF,
Hoffa fat pad. C, Axial MRI through the menisci shows the patellar tendon (PT),
popliteus tendon (P) and the medial (MH) and lateral heads (LH) of the
gastrocnemius. The popliteal artery (PA) and other neurovascular bundle structures
pass between the heads of the gastrocnemius. The PCL attaches to the posterior tibia
at this level. Fluid (F) is present in the lateral recess of the joint capsule.
The posteromedial and posterolateral corners help maintain the
multidirectional and rotational stability of the femur and tibia relative to each
other throughout the knee’s range of motion. The posteromedial corner is
composed of the structures between the MCL and the PCL, most importantly the
semimembranosus tendon and its various insertional expansions that strengthen
the posteromedial joint capsule. The posterolateral corner is supported by the
popliteus tendon, the LCL (fibular collateral ligament), the arcuate ligament, the
posterior capsule (and additional named capsular structures that we do not
routinely identify), as well as the popliteus, the biceps femoris, the lateral head
of the gastrocnemius muscles, and the IT band. The popliteus muscle originates
along the posterior aspect of the proximal tibia, and its tendon passes posterior to
the lateral meniscus (through the popliteus hiatus) to insert at the lateral aspect
of the lateral femoral condyle.
The synovial cavity envelops the medial, lateral, and patellofemoral
compartments, extends around and excludes the cruciate ligaments, and has a
large superior extension, the suprapatellar recess. There is normally a small
amount of joint fluid visible on MRI, often in one of the many recesses that
follow the contours of the joint. The presence and size of synovial recesses is
variable, but the most constant ones are the suprapatellar recess and the lateral
recess (Figure 5.4C).
•
FIGURE 5.5 Normal meniscal roots on axial MRI. A, The anterior and posterior
horns of the lateral meniscus (LM) attach to the intercondylar fossa anterior and
posterior to the lateral tibial tubercle (arrow), respectively. The anterior root of the LM
interdigitates with the distal anterior cruciate ligament (ACL) fibers. B, The anterior
root of the medial meniscus (MM) typically inserts into the anterior flat intercondylar
region of the tibial plateau. The posterior root of the MM attaches just anterior to the
posterior cruciate ligament (PCL) insertion.
•
FIGURE 5.6 Normal meniscal roots on coronal PD FS MRI. A, Anterior root of the
lateral meniscus (arrow) with a normal striated appearance. B and C, Posterior root of
the lateral meniscus (long arrow) and posterior root of the medial meniscus (short
arrow) near the posterior cruciate ligament (*). Ligament of Wrisberg (arrowheads).
The large fat pad that is inferior to the patella and posterior to the patellar
retinacula is the Hoffa fat pad. The quadriceps fat pad is small and triangular and
sits on top of the patella, behind the quadriceps tendon and in front of the
suprapatellar recess. The large fat pad between the suprapatellar recess and the
femur is the prefemoral fat pad (see Figure 5.2B).
•
FIGURE 5.7 Diagram of intermeniscal ligaments. A, Transverse (anterior) meniscal
ligament. B, Posterior intermeniscal ligament. C, Lateral oblique intermeniscal
ligament (extends from anterior horn of lateral meniscus to posterior horn of medial
meniscus). D, Medial oblique intermeniscal ligament (extends from anterior horn of
medial meniscus to posterior horn of lateral meniscus).
•
FIGURE 5.8 Transverse intermeniscal ligament. A, Axial PD FS MRI shows
transverse intermeniscal ligament (arrowheads) connecting the anterior horns of the
medial and lateral (arrow) menisci. The anterior root (*) of the lateral meniscus is
seen. There is an incidental Baker cyst. B, Sagittal PD FS MRI shows a cleft (arrow)
between the transverse intermeniscal ligament and the anterior horn of lateral
meniscus that may be mistaken for a meniscal tear. C, Sagittal PD FS MRI of a more
medial slice shows further separation of the transverse intermeniscal ligament
(arrowhead) and the anterior horn of the lateral meniscus (arrow).
The knee has medial, lateral, and patellofemoral articular compartments. The
medial compartment can be recognized on coronal MRI by the presence of the
MCL and greater subcutaneous fat thickness compared with the lateral
compartment. On sagittal MRI, the medial tibial plateau is concave upward and
the posterior horn of the MM is much wider than the anterior horn. On axial
MRI, the medial condyle and the medial tibial plateau are elongated anterior to
posterior. The lateral compartment can be recognized on coronal MRI by the
presence of the IT band, the LCL, the biceps tendon, and the fibula. On sagittal
MRI, the medial tibial plateau is convex upward and the posterior and anterior
horns of the lateral meniscus are about the same width. On axial MRI, the lateral
condyle and lateral tibial plateau are round. The patellofemoral compartment has
medial and lateral facets. On axial MRI, the medial patellar facet is typically
shorter than the lateral patellar facet, although there is some anatomic variation.
Hyaline articular cartilage generally has intermediate signal on MRI; the
layers that abut the subchondral bone have lower signal because they have less
water. The deepest layer of articular cartilage is calcified and abuts the
subchondral bone.
MENISCAL TEARS
The primary MRI findings of a meniscal tear are (1) high signal within the
normally dark meniscus that extends unequivocally to an articular surface and
(2) a variety of morphologic abnormalities. If a finding is seen on 2 adjacent or 2
anatomically correlated images, the tear should be diagnosed as present; if the
finding is seen on only 1 image, the tear should be reported as possibly
present.1–3 Previous meniscal surgery may mimic the morphology of meniscal
tears, so the surgical history is important. Meniscal tears should be described by
location, extent, and morphology. There is no generally accepted clinically
relevant imaging-based classification system.
Horizontal tears are oriented parallel to the inferior or superior surfaces of the
meniscus (Figure 5.9). Horizontal tears are commonly degenerative and are
frequently found in older patients with osteoarthritis. Meniscal cysts may form at
the periphery when joint fluid escapes through the meniscal tear (Figure 5.10).
Horizontal tears tend not to displace or cause mechanical symptoms, unless a
flap becomes displaced against the side of the femur (Figure 5.11).
•
FIGURE 5.9 Horizontal tear (arrow) of the posterior horn of the medial meniscus
extending into the inferior articulating surface on sagittal PD MRI.
•
FIGURE 5.10 Horizontal lateral meniscal tear. A, Sagittal and B, coronal PD FS
MRI show horizontal tear of the entire lateral meniscus with meniscal cyst formation
(arrow). C, Axial T2 FS at the level of the meniscus shows the cyst (arrow).
•
FIGURE 5.11 Lateral meniscal flap tear. A-D, Coronal PD FS MRI, anterior to
posterior, shows a horizontal tear of the body of the lateral meniscus with the torn
meniscus splayed apart against the lateral femoral condyle.
Longitudinal tears follow a circumferential course around the meniscus and

touch the superior and inferior articular surfaces. Longitudinal tears may also be
called circumferential or vertical tears (Figures 5.12 and 5.13). The appearance
on MRI depends on the imaging plane relative to the direction and location of
the tear. Because the cleavage plane follows the circumferential collagen
bundles, hoop strength may be intact, but loss of radial fibers may cause the
inner meniscal fragment to displace centrally. This displaced longitudinal tear is
called a bucket handle tear. Medial meniscal bucket handle tears tend to displace
centrally resulting in the double PCL sign (Figure 5.14). Lateral meniscal bucket
handle tears tend to displace anterocentrally, resulting in the double anterior horn
sign (Figure 5.15). Lateral bucket handle meniscal fragments may also displace
centrally, resulting in the double ACL sign (Figure 5.16).
Peripheral longitudinal tears of the lateral meniscus occur at the junction of
the ligament of Wrisberg with the posterior horn of the lateral meniscus and are
called Wrisberg rips. Wrisberg rips are typically associated with ACL tears and
can potentially be confused with a far lateral insertion of the Wrisberg ligament
(Figure 5.17).
•
FIGURE 5.12 Vertical medial meniscal tear (arrow) through the posterior horn on
sagittal PD FS MRI.
Radial tears begin at the free edge of the meniscus and propagate toward the
periphery, so that a complete radial tear traverses the full width of the meniscus
(Figure 5.18). They may occur anywhere within the meniscus. Because radial
tears disrupt the circumferential collagen bundles, the functional hoop strength
of the meniscus is lost. Axial loading of the femur against the tibia will result in
meniscal extrusion rather than hoop strain. The appearance of radial tears on
MRI depends on the location of the tear and the imaging plane, but the key
distinguishing feature from longitudinal tears is the involvement of the free
edge.4 Meniscal extrusion may not be evident because knee MRI is not typically
performed with weight-bearing.
•
FIGURE 5.13 Peripheral vertical medial meniscal tear. A, Sagittal and B, coronal
PD FS MRI show a longitudinal peripheral medial meniscal tear (arrows) involving the
body and posterior horn. There is also an anterior cruciate ligament tear (arrowhead)
and impaction fractures of the tibia (*) from pivot shift mechanism of injury.
•
FIGURE 5.14 Bucket handle meniscal tear. A, Axial T2 FS MRI shows a vertical
tear of the body and posterior horn of the medial meniscus with central displacement
of the free edge portion (arrows). B, Coronal T1 MRI shows the displaced meniscal
fragment (short arrow) adjacent to the posterior cruciate ligament (PCL) (long arrow).
C, Sagittal PD MRI shows the double PCL sign, with the displaced meniscal fragment
(short arrows) mimicking the orientation of the PCL (long arrow). The extra signal in
the proximal tibia is from previous anterior cruciate ligament reconstruction.
Injuries of the meniscal roots result in loss of meniscal hoop strength with
consequences similar to those of radial meniscal tears. Most meniscal root
injuries occur in the posterior roots, especially the posterior root of the MM.5
Tears of the posterior root of the MM are commonly degenerative, whereas tears
of the posterior root of the lateral meniscus are commonly acute and traumatic
(Figure 5.19). Posterior meniscal root injuries are typically radial tears. Direct
posterior root avulsions from the tibial plateau are less common, as are anterior
meniscal root tears. Meniscal root injuries may be managed conservatively or
treated surgically, with either partial meniscectomy or meniscal repair.
•
FIGURE 5.15 Acute knee injury with pain and locking. A, Sagittal PD MRI through
the lateral meniscus shows apparent enlargement of the anterior horn with diminutive
posterior horn. There is also an impaction fracture of the lateral femoral condyle (**).
B, A more central image shows the double anterior horn sign, with the torn fragment
(arrowhead) displacing the anterior horn (arrow) out of its normal position. Impaction
injury of the posterior tibia is present (*). C, Axial T2 FS MRI shows the torn fragment
(arrowhead) in relation to the anterior horn (arrow).
•
FIGURE 5.16 Bucket handle lateral meniscal tear. A, Sagittal PD FS through the
lateral compartment shows a small nondisplaced fragment of the posterior horn
(arrowhead). B, Sagittal PD FS through the intercondylar notch shows the displaced
fragment (arrow). C, Coronal PD FS shows the displaced fragment (arrow) adjacent
to the anterior cruciate ligament.
•
FIGURE 5.17 Wrisberg rip. A and B, Consecutive sagittal PD FS MRI shows a
peripheral longitudinal tear of the posterior horn of the lateral meniscus (arrows)
adjacent to the ligament of Wrisberg attachment. The tear demonstrates an irregular
contour and the apparent Wrisberg ligament attachment to the posterior horn of the
lateral meniscus extended four sagittal images beyond the posterior cruciate ligament
(not shown).
•
FIGURE 5.18 Lateral meniscus radial tear. A, Sagittal PD, B, axial T2 FS, and C,
coronal PD FS MRI show a radial tear (arrow) in the body of the lateral meniscus.
Meniscocapsular separation may occur with rotational injuries and is

associated with cruciate ligament tears.6 In addition to direct visualization of
meniscocapsular ligament tears, perimeniscal fluid and an irregular peripheral
meniscal margin are indicative of meniscocapsular separation (Figure 5.20).
Meniscal displacement relative to the tibia and meniscal corner tears may be
additional findings. At the meniscocapsular junction of the posterior horn of the
MM, small, smooth recesses that extend incompletely along the meniscal
periphery are a normal finding and should not be mistaken for a tear.6
•
FIGURE 5.19 Tear of the medial meniscal root. Coronal T2 FS MRI shows a
complete radial tear of the posterior root of the medial meniscus (arrow).
•
FIGURE 5.20 Meniscocapsular separation. Coronal T2 FS MRI. There is medial
meniscocapsular separation seen as a full-thickness tear of the meniscocapsular
ligament (long arrow). Medially, partial thickness tear of the meniscotibial (coronary)
ligament (arrowhead) and high-grade tear of the superficial layer of the medial
collateral ligament (MCL) are noted additionally (at this level, the meniscofemoral and
meniscotibial ligaments form the deep layer of the MCL). Observe the intact coronary
ligament (short arrow) in the lateral tibiofemoral compartment.
Meniscal detachment from the tibial plateau with associated disruption of the
meniscotibial (coronary) ligament results in a floating meniscus.7 On MRI, fluid
is seen between the floating meniscus and the opposing tibial plateau (Figure
5.21). The typical treatment for floating meniscus is surgical reattachment.
A discoid meniscus refers to a meniscus that is disc-shaped rather than C-
shaped (Figure 5.22). Common MRI criteria for lateral discoid meniscus include
(1) meniscal width more than 15 mm on coronal image or (2) more than 2 bow
ties (continuity of anterior and posterior horns) on 4- to 5-mm-thick sagittal
images.8 There may also be a rectangular shape on sagittal images if the central
portion of the bow tie is excessively thick. Impaired function may lead to
symptoms or tears (Figure 5.23). Partial discoid menisci are somewhere between
disk-shaped and C-shaped; sometimes the extra tissue is only a thin membrane.
Discoid menisci usually involve the lateral meniscus.
•
FIGURE 5.21 Floating medial meniscus (MM). Coronal T2 FS MRI in a 65-year-old
male demonstrates fluid (arrow) deep to the MM (compare with the lateral meniscus).
The menisci have limited capacity for healing and regeneration. Acute,
traumatic, simple, short peripheral tears in young patients have the best chance
of healing. Surgical options include direct repair, trimming of unstable edges and
fragments, and meniscectomy, but the role of arthroscopic meniscal surgery
remains controversial. Chronic, degenerative, complex, and central tears in older
patients have little chance of healing. Meniscal injuries usually lead to
osteoarthritis.
LIGAMENT INJURY BIOMECHANICS

Like the spinal column, the knee may be thought of as an articulated column
stabilized by surrounding soft-tissue structures. The joint capsule with its many
smaller named ligaments invests the entire knee and supports it on all sides. The
medial side is also supported by the MCL and medial retinaculum; the lateral
side by the LCL complex (IT band, LCL itself, biceps femoris tendon) and
lateral retinaculum; the anterior aspect by the structures of the quadriceps
mechanism; and the posterior aspect by the gastrocnemius muscles. The
posterolateral corner has the popliteus muscle and tendon and arcuate ligament,
whereas the posteromedial corner has the semimembranosus tendon and
posterior oblique ligament. The ACL and PCL occupy the central portion of the
knee, with the ACL lateral to the PCL.
When the extended knee is loaded by bending forces, the structures on the
concave side of the bend are compressed and the structures on the convex side
are distracted (Figure 5.24). Compressive injuries include bone bruises and
impaction fractures; distractive injuries include tears of ligaments, tendons,
muscles, and capsule or avulsions of their bony attachments. Under valgus
loading, an MCL injury is combined with lateral compartment bone bruises or
impaction fractures. If the loading is severe enough, the ACL and PCL also tear
under tension. Under varus loading, the LCL complex tears under tension and
the medial compartment sustains the compressive injury; with severe loading,
the ACL and PCL also tear. With hyperextension, the compressive injury
involves the contiguous anterior aspects of the femur and tibia and the tensile
injury involves the posterior capsule and gastrocnemius muscles; if there is
accompanying anterior or posterior translation of the tibia, the ACL or PCL may
tear, respectively. With hyperextension-valgus loading, the compressive injury is
anterolateral and the distractive injury involves the posteromedial corner, the
MCL, and the PCL. With hyperextension-varus loading, the compressive injury
is anteromedial and the distractive injury involves the posterolateral corner and
the ACL.
•
FIGURE 5.22 Discoid lateral meniscus. A, Coronal PD FS MRI shows the body of
the lateral meniscus extending to the intercondylar notch. B-E, Sagittal PD FS MRI,
lateral to medial, shows a discoid lateral meniscus that does not separate into anterior
and posterior horns (too many bow ties).
•
FIGURE 5.23 Discoid lateral meniscus with tear. A, Coronal and B, sagittal PD FS
MRI showing a discoid lateral meniscus with inferior surface tear (arrow).
When the flexed and externally rotated knee sustains valgus stress, the ACL
and the MCL are loaded under tension. If the ACL tears, the tibia is able to
translate anteriorly beneath the femur and impact the lateral condyle, resulting in
the pivot shift bone bruise pattern that is highly correlated with ACL tears. The
medial and lateral menisci, which act as buttresses against translation of the
knee, may also be torn. With weight-bearing or axial compression, meniscal
tears are more likely. The combination of tears of the ACL, the MCL, and a
meniscus (usually lateral) is called the unhappy triad; if both menisci are torn, it
is an unhappy tetrad. Much less commonly, varus stress on the internally rotated
and flexed knee may result in tears of the ACL and lateral and posterolateral
structures; the Segond fracture may be part of this injury complex.
•
FIGURE 5.24 Articulated column biomechanics. When the knee is struck from the
side, the nearer side is loaded under compression and the farther side is loaded
under tension. If the trauma is severe enough, the cruciate ligaments are also loaded
under tension. Courtesy of Tal Delman, MD.
•
FIGURE 5.25 Anterior cruciate ligament (ACL) tear. A, Sagittal PD FS MRI through
the intercondylar notch shows complete ACL tear at its femoral attachment and a
large joint effusion. B, Sagittal MRI through the lateral compartment shows typical
pivot shift bone bruises involving the lateral femoral condyle and the posterior lateral
tibial plateau.
ANTERIOR CRUCIATE LIGAMENT INJURY

The primary finding of an ACL tear on MRI is that the normal ACL will be
absent. In acute situations, there will be edema (high T2 signal) at the site and
fragments of the torn ACL may be seen (Figure 5.25). In chronic situations, the
ACL may simply be absent, replaced by fat and scar tissue. Incomplete ACL
tears may be evident as partial discontinuity or focal high T2 signal. The pivot
shift pattern of bone bruises is common in sports-related ACL injuries, where
bone bruises are located at the posterior tibia and the anterior portion of the
medial femoral condyle. Associated features of ACL tears include buckling of
the PCL and anterior translation of the tibia. Segond fractures may be evident on
radiographs (see Figure 3.21) but difficult to see on MRI. Cartilage and
osteochondral defects are common, particularly along the posterior tibia.
The ACL reconstruction is common among athletes at all levels. Bone-
tendon-bone autograft harvested from the middle third of the patellar tendon or
4-strand tendon graft harvested from the semitendinosus-gracilis tendons and
doubled over are threaded through tunnels in the lateral femoral condyle and
anteromedial tibia, following the path of the native ACL (Figure 5.26).9 The
ends are fixed to the femur and tibia using a variety of methods, including metal
and nonmetal implants. Synthetic materials or allografts may also be used
instead of tendon autografts.
Mucoid degeneration of the ACL may resemble low-grade ACL tears with
high T2 signal within its substance (Figure 5.27). This condition becomes more
common in older age groups. The abnormal signal tends to occupy the central
portion of the ligament and typically extends along its entire length.10 Partial
ACL tears tend to involve the periphery and be more focal.
•
FIGURE 5.26 Anterior cruciate ligament (ACL) reconstruction with hamstring
autograft. A-C, Sagittal PD MRI (lateral to medial) shows ACL reconstruction with
intact, robust tendon graft. Arthrofibrosis (arrow) is present anterior to the graft on the
lateral-most image (A).
POSTERIOR CRUCIATE LIGAMENT INJURY

PCL tears are typically seen on MRI as regions of focal discontinuity or high T2
signal.11 Midsubstance tears are most common. Tibial attachment injuries may
be soft-tissue or bony avulsions. In sports, the PCL may be ruptured by
hyperextension, medial or lateral bending, or severe rotation (Figure 5.28).
During motor vehicle accidents, the PCL is commonly injured by a posteriorly
directed blow to the tibia while in a flexed position, the dashboard injury (Figure
5.29). A fall on the flexed knee, striking the proximal tibia and posteriorly
translating the tibia relative to the femur, may result in the same injury as
striking the dashboard. A concurrent bone bruise at the anterior aspect of the
tibia indicates this mechanism of injury.
PCL injuries may occur in isolation but are common components of
multiligament knee injuries, including dislocations. PCL injuries are not
typically repaired or reconstructed except as a component of a multiligament
knee reconstruction.
Mucoid degeneration may resemble PCL tears (Figure 5.30)12 and has the
same imaging features as in the ACL.
•
FIGURE 5.27 Anterior cruciate ligament myxoid degeneration shown on sagittal T2
FS MRI. The high intrasubstance signal is surrounded by intact fibers.
•
FIGURE 5.28 Posterior cruciate ligament (PCL) injury. Sagittal T2 FS MRI shows
low-grade PCL sprain with increased intrasubstance signal but no discontinuity.
•
FIGURE 5.29 Dashboard posterior cruciate ligament (PCL) injury. A, Sagittal PD FS
MRI through the intercondylar notch shows complete tear of the PCL leaving only a
small tibial remnant. B, MRI through the lateral compartment shows anterior tibial
bone bruise from striking the dashboard during a car crash.
MEDIAL COLLATERAL LIGAMENT INJURY

Proximal MCL tears are more common than distal tears and may occur in
isolation or as a component of a more complex injury. Low-grade MCL tears are
evident on MRI as edema around the ligament. Higher-grade tears will show
edema, thickening of the ligament with high signal, and discontinuity (Figure
5.31). Distal MCL injuries may appear as a wavy or corrugated band of tissue at
the proximal tibial shaft.
Most MCL injuries are treated conservatively. Posttraumatic ossification of
the MCL, usually proximal, is termed Pellegrini-Stieda syndrome. Stieda
fracture refers to an avulsion fracture of the medial femoral condyle at the origin
of the MCL.
POSTEROLATERAL CORNER INJURY

The 3 important stabilizers of the posterolateral corner are the popliteus tendon,
the LCL, and the popliteal-fibular ligament. The popliteal-fibular ligament
connects the myotendinous junction of the popliteal tendon and the fibular head
and is not easily identifiable on routine knee MRI. The posterolateral corner
resists varus angulation and external tibial rotation. Injuries of the posterolateral
corner generally occur incidental to serious knee injuries involving multiple
structures (Figure 5.32); isolated injuries of individual posterolateral corner
structures are uncommon. On MRI, surrounding edema, thickening with high
signal, discontinuity, or absence of posterolateral corner structures may be
observed.13,14 It is particularly important to evaluate the popliteus tendon by
following its entire course, assess the LCL complex, and identify fibular head
avulsion fractures. Surgical repair of posterolateral corner injuries may be
performed when other knee injuries are reconstructed.
•
FIGURE 5.30 Posterior cruciate ligament (PCL) mucoid degeneration. Sagittal T2
FS MRI shows high signal within the PCL surrounded by intact peripheral fibers.
•
FIGURE 5.31 Medial collateral ligament (MCL) sprain. A, Coronal PD FS MRI
shows high-grade tear through the femoral attachment of the MCL with surrounding
edema and hemorrhage. B, Axial T2 FS MRI shows a few remaining MCL fibers
surrounded by fluid.
POSTEROMEDIAL CORNER INJURY

The primary structure to identify on MRI at the posteromedial corner is the
semimembranosus tendon insertion, which has several arms of attachment.15
There are several variable ligaments that may sometimes be distinguishable from
the posteromedial joint capsule. Injuries to the posteromedial corner structures
have the same nonspecific imaging appearance as other ligamentous and
tendinous injuries. Injuries of the posteromedial corner generally occur
incidental to other injuries that may be more obvious clinically, especially to the
ACL, MCL, or PCL (Figure 5.33). Posteromedial corner injuries are associated
with anteromedial rotational instability, in which there is excessive anterior
translation of the medial tibial plateau and widening of the medial joint space
with external rotation. Surgical repair of the posteromedial corner may be
performed when other knee injuries, particularly ACL and PCL tears, are
reconstructed.
•
FIGURE 5.32 Posterolateral corner injury in a 26-year-old man with hyperextension
injury from jumping off a fence and landing badly. A, Sagittal PD FS MRI shows
anterior tibial bone bruise and edema in the popliteus muscle belly (arrow). The
popliteus tendon is not apparent. It is difficult to identify the posterior joint capsule and
related structures. B, Coronal PD FS MRI shows complete tears of the lateral
collateral ligament, popliteus tendon, and biceps femoris tendon. There are also
complete tears of the anterior cruciate ligament and posterior cruciate ligament. The
lateral knee capsule is torn, but the medial collateral ligament is intact.
•
FIGURE 5.33 Posteromedial corner injury. A, Sagittal PD FS MRI shows anterior
impaction fractures of the medial femoral condyle and medial tibial plateau from
hyperextension. The posterior capsule is not identifiable below the joint line and is
presumably torn (arrowheads). There are tears of the medial head of the
gastrocnemius and the semimembranosus. B, Coronal PD MRI shows the tear of the
distal semimembranosus (arrow).
•
FIGURE 5.34 Catastrophic knee injury in a pedestrian struck by a car from the
lateral side, forcing the knee into severe valgus. A, Coronal PD FS MRI shows a
complete tear of the medial collateral ligament (black arrow) with lateral femoral
condyle bone bruise (white arrow). B, Sagittal PD MRI shows tear of the anterior
cruciate ligament (white arrow). C, Sagittal PD MRI shows tear of the posterior
cruciate ligament (black arrow).
MULTILIGAMENT INJURY
Catastrophic multiligament injuries, in which both ACL and PCL are torn, are
typically the result of high-energy trauma, such as injuries in motorized vehicle
crashes or falls from substantial heights.16 There may be tensile injuries on one
side of the knee and compression injuries on the other. Pedestrians struck by cars
may sustain these types of injuries (Figures 5.34 and 5.35). Purely tensile
injuries are also possible if one side of the knee separates without compressing
the opposite side. Purely compressive injuries such as tibial plateau or distal
femur fractures tend to spare the major ligaments.
EXTENSOR MECHANISM INJURY

Jumper’s knee is an athletic overuse syndrome affecting the infrapatellar tendon
and its attachments. Any activity with jumping may cause or aggravate the
condition. In adults, jumper’s knee is infrapatellar tendinopathy thought to result
from chronic repetitive stress at the inferior pole of the patella; an alternate
theory is that the inferior pole of the patella impinges on the tendon during knee
flexion, resulting in tendinosis. On MRI, the tendon may be thickened and show
increased T1 and T2 signals, often resembling a hair comb on axial images
(Figure 5.36).17 The most common region affected is the posterior aspect of the
tendon adjacent to the inferior pole of the patella. Bursal fluid between the
tendon and the tibia may be present.
•
FIGURE 5.35 Catastrophic knee injury in a pedestrian struck by a car from the
medial side, forcing the knee into severe varus. A, Coronal T2 FS MRI shows
complete tear of the lateral collateral ligament complex (black arrow) with medial tibial
bone bruise (white arrow). B, Sagittal PD FS MRI shows tear of the anterior cruciate
ligament (white arrow). C, Sagittal PD FS MRI shows tear of the posterior cruciate
ligament (white arrow).
•
FIGURE 5.36 Jumper’s knee. A, Axial T2 FS MRI through the proximal infrapatellar
tendon shows thickening and comblike high signal (arrow). B, Sagittal PD FS MRI
shows partial thickness tear (arrow) of the infrapatellar tendon. The proximal half of
the tendon is thickened.
•
FIGURE 5.37 Patellar tendon tear. Sagittal T1 MRI shows complete tear through
the proximal infrapatellar tendon. Both the infrapatellar and quadriceps tendons show
tendinopathy.
Infrapatellar tendon ruptures are athletic injuries that occur during jumping
sports such as the triple jump in track and field (Figure 5.37). The knee cannot
be extended. On radiographs, patella alta is present. On MRI, the location of the
tear and the quality of the tendon can be assessed; underlying tendinosis is
common. The treatment is surgical.
In older adults, quadriceps tendon tears are more likely than infrapatellar
tendon injuries. Quadriceps tendon tears often occur just proximal to the patella,
usually through a region of preexisting tendinopathy (Figure 5.38). With
complete tears, the knee cannot be extended, and patella baja may be evident on
radiographs. With partial tears, there is weakness and pain with attempted
extension.
LATERAL PATELLAR DISLOCATION

Patellar dislocations are typically lateral and may occur with flexion and internal
rotation of the femur on a fixed tibia. After the dislocation, the quadriceps may
extend to the knee and pull the patella back into the trochlear groove, so that by
the time the injury event is over, the dislocation has already been reduced and
the patient may not realize that the dislocation has occurred. On MRI, impaction
injuries of the medial patella and lateral femoral condyle have a characteristic
appearance (Figure 5.39), and associated tears of the medial patellofemoral
ligament, the medial retinaculum, the MCL, and the ACL may be found.18
Avulsion fractures at the attachment of the medial patellofemoral ligament may
occur, usually at the medial margin of the patella. Chondral or osteochondral
fractures may involve either the patella or femoral trochlea, sometimes with
displaced fragments.
•
FIGURE 5.38 Quadriceps tendon tear. Sagittal PD MRI shows discontinuity of the
tendon (arrow) at the superior pole of the patella.
•
FIGURE 5.39 Reduced lateral patellar dislocation. Axial T2 FS MRI shows
characteristic bone bruises at the medial patellar facet and the lateral aspect of the
lateral femoral condyle.
BONE BRUISE PATTERNS

The specific pattern of bone bruises seen on MRI may suggest the mechanism of
injury19 and the associated injuries: Kissing contusions of a femoral condyle and
tibial plateau (adjacent bruises or impaction fractures) indicate a bending injury
to the extended knee; the opposite side will typically sustain distraction injuries.
Bending injuries include varus, valgus, and hyperextension. The pivot shift
pattern (bruises or impaction fractures of the lateral femoral condyle and
posterolateral tibia) occurs with ACL tears; MCL and meniscal tears are
commonly associated. Isolated bruises of the anterior aspect of the tibia may
indicate a dashboard injury with PCL tear. Bruises of the medial facet of the
patella and lateral femoral condyle may indicate previous lateral patellar
dislocation.
ARTICULAR CARTILAGE INJURY

Injuries to the articular cartilage are common. Articular cartilage has only
limited ability to heal. Radiographs and CT will not show these injuries until
posttraumatic osteoarthritis is well advanced, often years later. Some articular
cartilage injuries may be demonstrated by MRI when there are morphologic
abnormalities (Figures 5.40 and 5.41). Osteochondral injuries are sometimes
evident by abnormal signal in the injured bone, even as the overlying cartilage
may appear normal (Figure 5.42). Displaced cartilage or osteochondral
fragments may become loose bodies (Figure 5.43).
Surgical techniques for treating articular cartilage lesions include arthroscopic
debridement and smoothing the articular surface, microfracture (to stimulate
healing), mosaicplasty (autograft of multiple small osteocartilaginous plugs),
autologous chondrocyte transplantation, cadaver osteochondral allograft, cell-
free implants, and finally, total joint replacement.20
MYOTENDINOUS INJURY
Muscle tendon injuries (strains) about the knee are frequent accompaniments to
catastrophic trauma. Isolated muscle injuries may occur in the thigh or calf, often
from athletic activities or falls. Low-grade strains may be seen on MRI as
muscle edema, typically around muscle tendon junctions. Higher-grade injuries
may show actual discontinuities of the muscle tendon unit, hematoma, or
retraction (Figure 5.44). Muscle strains about the knee most commonly occur in
the medial gastrocnemius and the soleus. Hematomas are common with calf
injuries. Chronic injuries may be associated with disuse atrophy, myositis
ossificans, and calcific myonecrosis.
•
FIGURE 5.40 Traumatic full thickness cartilage injury. Axial T2 FS MRI shows a
focal osteochondral injury (arrow) of the medial patellar facet.
•
FIGURE 5.41 Traumatic full-thickness cartilage defect. A-C, Coronal, sagittal, and
axial PD FS MRI show a focal cartilage defect (arrows) in the lateral femoral condyle,
filled with fluid.
•
FIGURE 5.42 Traumatic osteochondral injury of the posterior aspect of the lateral
femoral condyle shown on sagittal PD FS MRI.
•
FIGURE 5.43 Osteochondral loose body. A, Coronal T2 FS MRI shows the site of
an osteochondral fracture (arrow) of the lateral femoral condyle. B, Sagittal T1 MRI
through the lateral compartment shows that the osteochondral fragment (arrow) has
displaced anterior to the femoral condyle.
•
FIGURE 5.44 A, Sagittal PD FS and B and C, axial T2 FS MRI show high-grade
strain of the gastrocnemius muscle.
•
FIGURE 5.45 Plica syndrome. A, Axial T2 FS MRI through the midpole of the
patella shows a medial plica (arrow) interposed between the trochlea and medial
patellar facet, outlined by joint effusion. B, Sagittal PD FS MRI shows the extent of the
plica (arrow), just posterior to the patella.
MISCELLANEOUS KNEE SYNDROMES

Plica Syndrome
A plica is an infolding or ridge on the inner surface of the joint lining and is
thought to result from incomplete involution during embryologic development of
the joint.21 Most common on the medial side of the joint, a plica may impinge on
the patellofemoral joint, disrupt normal tracking of the patella, or tether the
quadriceps mechanism, resulting in plica syndrome. MRI findings are often
normal but may include thickening or inflammation of the plica (Figure 5.45),
perhaps even a pseudomass or adjacent osteochondral abnormality where there is
chronic impingement. Treatment of plica syndrome is conservative or
arthroscopic resection.
Iliotibial Band Syndrome

The IT band is a condensation from the tensor fascia latae with a tendinous
insertion on the femur and a ligamentous insertion on the tibia. The IT band
rotates rather than truly slides over any structures. MRI findings include edema
deep to the distal portion of the IT band as it traverses the lateral femoral
condyle and rarely, thickening of the IT band (Figure 5.46).22 IT band syndrome
is frequently described not only in long-distance runners and cyclists but also in
other athletic participants.
Fat Pad Edema

Edema involving the superolateral portion of Hoffa fat pad has been associated
with patellofemoral malalignment and patellar tendon-lateral femoral condyle
friction syndrome. Impingement of Hoffa fat pad between the inferior patella
and the lateral femoral condyle results in anterior knee pain. On imaging, patella
alta and lateral patellar subluxation may be found, in addition to fat pad edema
(Figure 5.47). Chondromalacia and eventually osteoarthritis may occur. It is
unclear whether the syndrome of infrapatellar fat pad impingement called Hoffa
disease (or hoffitis)23 is the same condition.
Edema involving the quadriceps (also called suprapatellar) fat pad is a
common finding on MRI but does not appear to be associated with anterior knee
pain or the conditions that may cause it, including patellofemoral malalignment
or patellofemoral osteoarthritis.24
•
FIGURE 5.46 Iliotibial (IT) band syndrome. Coronal PD FS MRI shows edema
along the superficial (arrow) and deep surfaces of the IT band.
Pes Anserinus Bursitis

Pes anserinus (goose’s foot) is the anatomical term that refers to the conjoined
tendons of the sartorius, gracilis, and semitendinosus, anterior to posterior, as
they insert at the medial proximal tibia superficial to the distal MCL. The
conjoined distal tendon would be the goose’s hindfoot, whereas the 3 diverging
tendons would correspond to the goose’s diverging toes. The pes anserinus bursa
is variable but typically found between these tendons and the tibia or between
the tendons and the distal MCL. Pes anserinus bursitis is thought to result from
friction and bursal irritation as the semitendinosus and gracilis tendons impinge
against the tibia during motion. Patients present with medial knee pain and often
have other internal derangements. On MRI, an enlarged fluid-filled bursa will be
present at the characteristic location (Figure 5.48).25
•
FIGURE 5.47 Hoffa disease. Sagittal T2 FS MRI shows extensive edema in the
infrapatellar fat pad with bowing of the infrapatellar tendon from mass effect.
•
FIGURE 5.48 Pes anserinus bursitis. A and B, Sagittal PD MRI through the medial
knee shows the pes anserinus tendons passing over an enlarged bursa distended
with fluid.
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1. Which structure is considered part of the posteromedial corner of the knee?

A. Arcuate ligament
B. Biceps femoris tendon
C. Lateral collateral ligament
D. Semimembranosus tendon
2. Which bone marrow edema pattern on knee MRI is most closely associated
with ACL tear?
A. Lateral patella, medial femoral condyle
B. Medial patella, lateral femoral condyle
C. Posterior tibial plateau, lateral femoral condyle
D. Anterior tibial plateau, medial femoral condyle
3. Which type of meniscal tear is most likely to result in loss of hoop strength
and meniscal extrusion?
A. Horizontal
B. Longitudinal
C. Radial
D. Meniscocapsular
4. A pedestrian crossing a street is struck from the side by a car at low speed,
injuring the right knee. Right knee MRI was subsequently performed. Which
injury most strongly suggests that the car approached from the pedestrian’s
left?
A. MCL tear
B. LCL tear
C. ACL tear
D. PCL tear

1. D The semimembranosus is the primary structure stabilizing the
posteromedial corner. The other options are components of the posterolateral
corner.
2. C With ACL injury, the tibia may translate anteriorly with the posterior tibial
plateau impacting on one or both femoral condyles.
3. C Radial tears disrupt the circumferential collagen bundles.
4. B The description indicates varus loading, resulting in tension injury of the
lateral knee.
6
MRI of Shoulder Injuries
Luis S. Beltran
It is important to be familiar with the normal anatomic and pathologic MRI

appearances of the structures in the shoulder to effectively diagnose and treat
traumatic and sports-related injuries. This chapter provides an introduction to the
various MRI techniques to evaluate the shoulder and the most common types of
injuries and is a good starting point for further inquiry into this interesting and
important anatomic region.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of MRI of shoulder injuries, the learner will be able
to
4. summarize relevant concepts and knowledge for the following topics: glenohumeral instability,
glenoid labral tears, rotator cuff tears and tendinosis, subacromial-subdeltoid bursitis, biceps
tendon pathology, and acromioclavicular joint (ACJ) injuries.
MRI SHOULDER PROTOCOL

For a routine shoulder MRI, the patient is placed supine in the MRI scanner, and
the arm is placed with the hand supinated and the thumb facing outward. A
sandbag is placed on the hand to maintain the position if the patient can tolerate
this. For optimal signal in the joint, a phased array shoulder coil is placed snugly
on the shoulder. If the shoulder coil is too small for the patient because of large
body habitus, a body phased array coil can be used instead. The MRI sequences
may vary from institution to institution, but, generally, we perform coronal
oblique proton density (PD), coronal oblique fat saturated T2 (FST2), sagittal
T1, sagittal FST2, and axial fat saturated PD sequences. If the patient has metal
hardware, the protocol should be altered to minimize metal artifacts, which
includes increasing the turbo factor and bandwidth, increasing the number of
excitations, and decreasing the slice thickness. Furthermore, fat saturation should
not be used and, instead, short tau inversion recovery (STIR) sequences should
be used to obtain fat suppression because STIR is less susceptible to metal
artifacts compared with fat saturation techniques.
MR arthrography is usually performed to evaluate the labrum, but it can also
help evaluate the joint capsule and rotator cuff. The patient is injected with a
gadolinium contrast mixture into the glenohumeral joint followed by MRI (see
chapter 29). At NYU, we usually obtain coronal oblique T1 FS, coronal oblique
T2 FS, sagittal T1, axial T1 FS, and oblique axial T1 FS MRI, with the arm in
abduction and external rotation (ABER) position. The ABER position has the
patient’s hand (on the affected side) behind the head or neck with the elbow
flexed. This position stretches out the anterior-inferior glenohumeral joint
capsule and labrum therefore optimizes evaluation of this region for imbibition
of contrast material into the labrum, increasing the detection of subtle labral
tears.1
DICTATION CHECKLIST
Our dictation checklist for shoulder MRI includes bones and bone marrow, joint
alignment, articular cartilage, rotator cuff, long head of the biceps tendon
(LHBT), labrum, glenohumeral ligaments, joint fluid and synovium, bursal fluid,
muscles, ACJ, coracoclavicular and coracoacromial ligaments, vessels and
nerves, focal lesions, cysts and masses, and subcutaneous tissues. Each of these
sets of structures should be identified and evaluated for morphology and signal
characteristics. Any region of high T2 signal should attract further scrutiny. The
clinical indication should be specifically addressed.
GLENOHUMERAL JOINT ANATOMY

The glenohumeral joint is a multiaxial synovial ball-and-socket joint formed by
the articular surfaces of the humeral head representing the ball and the glenoid
fossa representing the socket portions of the joint, likened to a golf ball on a tee.
This joint is the most mobile joint in the human body2 with tremendous range of
motion including adduction, abduction, flexion, extension, internal rotation,
external rotation, and 360° circumduction (Figure 6.1). This wide range of
motion, however, comes with the price of making the shoulder a relatively
unstable joint.2 This instability is alleviated by the reinforcing surrounding
structures, a combination of static stabilizers and dynamic stabilizers working in
synchrony to maintain shoulder stability while performing activities such as
extreme sports exertion or heavy manual work. The static stabilizers include the
glenohumeral joint capsule, ligaments, and glenoid labrum. The dynamic
stabilizers include the rotator cuff muscles and tendons and the long head of the
biceps brachii muscle and tendon.
•
FIGURE 6.1 Glenohumeral joint dynamics. Illustration of the glenohumeral joint
from a front view (top row) and side view (bottom row) demonstrating the wide range
of motion of the joint including internal rotation, external rotation, adduction,
abduction, flexion, extension, and 360° circumduction.
The glenoid articular surface is composed of hyaline cartilage and has a

distinct pear-shaped morphology, which is best appreciated from the side view or
sagittal projection on MRI. The glenoid is normally slightly retroverted or facing
posteriorly by an average of 7°.3 This shape is essential to maintain shoulder
stability. The humeral head articular surface is also covered by hyaline cartilage.
The morphology of the humeral head particularly along the superior and
posterior aspect is essential for the stability of the glenohumeral joint.
LABRUM AND GLENOHUMERAL LIGAMENTS

The glenoid labrum is a rim of fibrocartilage that is attached to the bony surface
of the glenoid rim and surrounds the periphery of the glenoid hyaline cartilage
articular surface (Figure 6.2). The labrum usually has uniformly low signal
intensity on all MR pulse sequences because of a short T2 relaxation time, which
is attributed to a homogenous composition of fibrocartilage. However, normal
variations in signal intensity including globular and linear increased signal,
particularly with intermediate-weighted PD sequences and older individuals,
have been described and attributed to variations in the composition of
fibrocartilage.4,5 The labrum usually has a triangular morphology; however,
other morphologies have also been described, including rounded, flat, cleaved,
notched, or absent.6 A conventional 3 Tesla (3T) MRI study without intra-
articular contrast may be sufficient to evaluate for a labral tear because of the
high signal-to-noise ratio obtained at 3T. Nevertheless, MR arthrography is still
the study of choice to evaluate the labrum7 because it distends the joint with
contrast material, increasing the detection of labral tears.
The depth of the glenoid fossa is increased by 50% by the glenoid labrum,
thereby contributing to the stability of the joint.6 It also serves as an attachment
point for the glenohumeral ligaments, the joint capsule, and the LHBT (Figure
6.3). The superior glenohumeral ligament (SGHL) and the LHBT attach to the
superior labrum. The biceps-labral complex describes the attachment of the
LHBT to the superior labrum. The middle glenohumeral ligament attaches to the
anterior superior labrum. The inferior glenohumeral ligament (IGHL) complex
consists of an anterior band, which attaches to the anterior-inferior labrum, a
posterior band, which attaches to the posterior inferior labrum, and an
intervening axillary pouch, which is the inferior part of the glenohumeral joint
capsule surrounding the joint. The labrum is firmly attached to the posterior and
inferior portions of the glenoid rim. Along the superior and anterior superior
portion of the glenoid rim, the attachment is less firm and has substantial
variation in the normal anatomy, which can be misdiagnosed by the
unaccustomed reader as a labral tear, as it is often filled with fluid or contrast on
MR images, mimicking a tear. The anatomic variants in this region of the labrum
include (1) the sublabral recess or sublabral sulcus, (2) the sublabral foramen or
sublabral hole, and (3) the Buford complex.
•
FIGURE 6.2 Normal labrum. A, Illustration of the normal labrum (dashed arrow)
consisting of a rim of fibrocartilage that is attached to the bony surface of the glenoid
rim (G) and surrounds the periphery of the glenoid hyaline cartilage articular surface.
The coracoid process (Cor) is located anteriorly, and spine of the scapula (S) and
acromion (Acr) are located posteriorly. B, Coronal FST1 MR arthrogram image
demonstrating a normal superior labrum with homogenously hypointense signal and
smooth triangular morphology in cross section (dashed arrow). H, humerus.
The sublabral recess (Figure 6.4), which is also referred to as a sublabral

sulcus, is a space between the biceps-labral complex and the superior portion of
the glenoid fossa. This space is the result of a synovial reflection medial to the
superior edge of the glenoid rim at the site of the insertion of the long head
biceps tendon on the supraglenoid tubercle, showing a loose attachment of the
superior labrum to the superior glenoid cartilage.8 Commonly, the portions of the
labrum are described by projecting the face of a clock onto the glenoid labrum
from the side view in which 12:00 is located at the biceps-labral complex, 3:00
is located anteriorly, 6:00 is located inferiorly, and 9:00 is located posteriorly.
Using this clockface method, the sublabral recess is located mostly between the
11- and 1-o’clock positions along the superior glenoid underlying the biceps-
labral complex. On coronal MRI images, the normal sublabral recess is present
in the superior aspect of the glenoid rim and is pointing toward the medial side
of the glenoid. This stands in contrast to an abnormal labral tear in this region
referred to as superior labrum anteroposterior (SLAP) lesion where the lesion
points toward the lateral aspect of the superior labrum.9
The sublabral foramen (Figure 6.5), which is also referred to as a sublabral
hole, is a localized normal detachment of the labrum from the underlying
glenoid rim, which is found in about 10% of asymptomatic subjects.10 When
present, it is located between the 1- and 3-o’clock positions along the glenoid,
anterior to the biceps-labral complex. A sublabral foramen should not be
confused with a tear of the anterior or superior labrum, which can have a similar
appearance. The slight differences in location and morphology are key in making
the correct diagnosis. A normal sublabral foramen should be limited to the
anterior superior labrum, it should not be displaced by more than 1 to 2 mm, and
it should have smooth borders.6 In contrast, a labral tear in this region will
typically be more prominent and have irregular borders and may or may not
extend into other portions of the labrum.
The Buford complex (Figure 6.6) refers to a prominent or cordlike and
thickened frayed middle glenohumeral ligament in association with absent
anterosuperior labrum. This normal variant is present in 1.5% to 2% of healthy
subjects.11
ROTATOR CUFF
The rotator cuff muscles and tendons include the supraspinatus, infraspinatus,
subscapularis, and teres minor (Figure 6.7). The suprapinatus muscle originates
from the supraspinatus fossa of the scapula. The infraspinatus muscle originates
from the infraspinatus fossa and the inferior surface of the spine of the scapula.
The teres minor muscle originates from the lateral border of the scapula. The
subscapularis muscle originates from the subscapularis fossa. The muscles and
tendons of the rotator cuff approximate each other along their insertion sites to
the humeral head. The subscapularis tendon inserts primarily at the lesser
tuberosity of the humeral head. The supraspinatus, infraspinatus, and teres minor
tendons insert at the greater tuberosity. The greater tuberosity has superior,
middle, and inferior facets. The supraspinatus tendon inserts primarily at the
superior facet and the infraspinatus tendon inserts primarily at the middle facet.
These 2 tendons interdigitate, fuse, and have a partly continuous attachment at
the margin of the superior and middle facets.9 The teres minor tendon inserts at
the inferior facet. The subscapularis tendon and supraspinatus tendon also have
some tendon fibers that fuse with each other over the bicipital groove between
the greater and lesser tuberosity, which helps to maintain the LHBT in its normal
location within the groove.12
•
FIGURE 6.3 Normal glenohumeral ligaments. A, Illustration of the glenohumeral
ligaments and joint capsule with front and cross-sectional side views. B, Sagittal T1
MR arthrogram image. C, Axial FST1 MR arthrogram image (superior aspect of joint).
D, Axial FST1 MR arthrogram image (middle aspect of joint). E, Axial FST1 MR
arthrogram image (inferior aspect of joint). The glenohumeral ligaments are attached
to the glenoid labrum (dashed arrow) medially and humeral head laterally and are
continuous with the joint capsule (arrowhead). The superior glenohumeral ligament
(SGHL) and long head of the biceps tendon (LHBT) attach to the superior labrum.
The middle glenohumeral ligament (MGHL) attaches to the anterior superior labrum.
The inferior glenohumeral ligament (IGHL) complex consists of an anterior band
(aIGHL), which attaches to the anterior-inferior labrum, a posterior band (pIGHL),
which attaches to the posterior inferior labrum, and an intervening axillary pouch (AP),
which is the inferior part of the joint capsule. The coracoid (Cor) is located anteriorly
and acromion (Acr) is located posteriorly. Clv, clavicle.
•
FIGURE 6.4 Sublabral recess. A, Illustration showing the normal variant sublabral
recess or sublabral sulcus (arrows) located mostly between the 11- and 1-o’clock
positions along the superior glenoid underlying the biceps-labral complex
(arrowhead). B, Coronal fat saturated T2 MR image showing the normal sublabral
recess (arrow) as hyperintense fluid signal in the superior aspect of the glenoid rim
interposed between the labrum and the glenoid articular cartilage and is pointing
toward the medial side of the glenoid. There is also normal expected hyperintense
fluid signal interposed between the superolateral border of the labrum and the
underlying biceps tendon at the biceps-labral complex (arrowhead) as there is
normally a small gap between these 2 structures.
The rotator cuff muscles are important dynamic stabilizers of the shoulder.
The supraspinatus abducts the shoulder and synergistically functions throughout
the range of abduction with the deltoid muscle. In the absence of supraspinatus
function, a substantial increase in force from the deltoid muscle is needed to
initiate arm abduction.13 The infraspinatus and teres minor externally rotate the
shoulder. The subscapularis internally rotates the shoulder and adducts the arm.
Coupling of forces from the rotator cuff muscles and tendons in both the
coronal and transverse planes is important for stabilizing the glenohumeral joint.
During abduction and overhead movement of the arm, the coupled forces of the
deltoid and the supraspinatus are directed toward the glenoid, which compresses
the humeral head against the glenoid and improves the stability of the joint.14
This is the predominant mechanism resisting superior humeral head
displacement. The additional force coupling between the anteriorly stabilizing
subscapularis and the posteriorly stabilizing infraspinatus also helps to maintain
the joint centered throughout the range of motion.14
•
FIGURE 6.5 Sublabral foramen. A, Illustration from front view. B, Axial FSPD MR
image showing the sublabral foramen or sublabral hole (arrow) with a small area of
increased MR signal due to small fluid-filled gap between labrum and the glenoid
along the 1- and 3-o’clock positions of the glenoid, anterior to the biceps-labral
complex (arrowhead).
•
FIGURE 6.6 Buford complex. Illustration (A) and axial FST1 MR arthrogram image
(B) of the Buford complex with a prominent or cordlike thickened and frayed middle
glenohumeral ligament (MGHL) (arrow) in association with absent anterosuperior
labrum (arrowhead).
The rotator cuff tendons usually have low signal on all MR pulse sequences;
however, there is often focally increased signal in the supraspinatus tendon at the
distal tendon insertion on coronal MR sequences where the tendon has an
oblique course, as it wraps over the greater tuberosity of the humeral head
because of magic angle artifact. This can be confused with tendinopathy if the
reader is not familiar with this artifact. Magic angle artifact occurs only in MR
pulse sequences with a relative short to intermediate time to echo (TE) such as
T1 and PD sequences; therefore, one should not see it on long TE sequences
such as an FST2-weighted image. If magic angle artifact is suspected as the
cause of increased signal on a short TE sequence, this should be confirmed by
the absence of increased signal on a FST2 sequence.
•
FIGURE 6.7 Normal rotator cuff. Illustration (A) and coronal fat saturated T2 (FST2)
(B), axial FSPD (C), sagittal FST2 (D), and sagittal T1 MR (E) images of the rotator
cuff muscles and tendons. The subscapularis tendon (Sub) inserts at the lesser
tuberosity (LT). The greater tuberosity (GT) has superior, middle, and inferior facets.
The supraspinatus tendon (Sup) inserts primarily at the superior facet (SF), the
infraspinatus tendon (Inf) inserts primarily at the middle facet (MF), and the teres
minor tendon (Ter) inserts at the inferior facet (IF). Between the lesser tuberosity and
greater tuberosity sits the bicipital groove (*). S, spine of the scapula.
LONG HEAD OF THE BICEPS TENDON

The biceps brachii muscle is composed of 2 heads: the short head, which
originates at the coracoid process of the scapula, and the long head, which
usually originates at the supraglenoid tuberosity and the superior labrum (Figure
6.8). Both heads insert at the radial tuberosity in the proximal radius at the
elbow. The LHBT has an oblique intra-articular course in the anterior superior
aspect of the glenohumeral joint through a space called the rotator interval, and
then the tendon makes a 30° to 45° turn along the anterior aspect of the humeral
head where the tendon becomes extra-articular as it courses within the bicipital
groove between the greater and lesser tuberosity.15–17 The origin of the LHBT
along the superior labrum is referred to as the bicipital-labral complex or biceps
anchor. There is normal variant anatomy of this attachment referred to as a
sublabral recess or sulcus, which can be mistaken as a labral tear and/or tendon
tear; therefore, one should be familiar with this. This is described in further
detail in the labrum portion of this chapter.
•
FIGURE 6.8 Normal biceps brachii muscles and tendons. Illustration of the long
head of the biceps brachii muscle and tendon (LHBT) originating at the supraglenoid
tuberosity (ST) and the short head of the biceps brachii muscle and tendon (SHBT)
originating at the coracoid process (Cor). Both tendons insert together in the elbow at
the radial tuberosity (RT).
The function of the LHBT and maintenance of its normal anatomic position
within the bicipital groove depends on the integrity of various surrounding
stabilizing structures. The static stabilizers include the anterosuperior
glenohumeral joint capsule (also referred to as the rotator interval capsule), the
SGHL, the coracohumeral ligament (CHL), and the transverse humeral ligament.
The dynamic stabilizers include the supraspinatus and subscapularis tendons.
Together, these stabilizing structures form a complex to insert along the greater
and lesser tuberosity over the bicipital groove maintaining the biceps tendon in
its anatomic location and are referred to as the biceps reflection pulley16–18
(Figure 6.9). The biceps reflection pulley limits medial subluxation of the LHBT
when the arm is abducted and externally rotated. Injuries to any of these
components are referred to as “pulley lesions.”19,20
ACROMIOCLAVICULAR JOINT
The ACJ is a plane synovial joint formed by the lateral surface of the clavicle
and the medial surface of the acromion, which are covered by hyaline articular
cartilage. There is an intervening small fibrocartilaginous disk that has the shape
of a meniscus, which allows only gliding movement of the joint. The stability of
the joint depends on the static stabilizing capsule and ligaments and the dynamic
stabilizing muscles surrounding the joint.6 The joint capsule surrounds the joint
and is firmly attached to the bony margins of the clavicle and acromion (Figure
6.10). The superior and inferior acromioclavicular ligaments reinforce the joint
capsule along the superior and inferior aspects of the joint, respectively, and can
be thought of as focal thickenings of ACJ capsule. The coracoclavicular
ligament consists of the conoid and trapezoid ligaments. The conoid ligament is
triangular in shape and medially located at its origin along the coracoid process
of the scapula and runs upward, forming an inverted cone as it widely attaches to
the undersurface of the clavicle. The trapezoid ligament has a quadrilateral
shape, is laterally located at its origin along the coracoid process, and runs
laterally and horizontally, attaching to the underside of the clavicle. The
coracoacromial ligament originates from the lateral aspect of the coracoid
process and inserts at the anterior aspect of the acromion. The deltoid muscle
attaches to the anterior aspect of the distal clavicle and the anterior and lateral
aspects of the acromion and spine of the scapula. The trapezius muscle attaches
to the posterior and superior aspects of the distal clavicle and acromion and
spine of the scapula. These 2 muscles together provide dynamic stabilization of
the ACJ.
SUBACROMIAL-SUBDELTOID BURSA
Bursae are small fluid-filled pouches lined by synovium and normally contain a
thin film of synovial fluid, which serves the purpose of alleviating friction by
creating a fluid-filled space between 2 tightly apposed structures that move
relative to one another. There are several bursae around the joints of the
shoulder, including the subacromial-subdeltoid (SA-SD) bursa, subcoracoid
bursa, coracoclavicular bursa, and supra-acromial bursa. Fluid often also collects
deep into and around the superior margin of the subscapularis tendon and is
often referred to as the subscapularis bursa; however, this almost always
communicates with the glenohumeral joint and is therefore considered by many
to be a normal joint recess rather than a true bursa.21 Mild distension of this joint
recess with physiologic joint fluid can be a normal finding on MRI, which does
not represent a bursitis.
•
FIGURE 6.9 Normal biceps reflection pulley. A, Illustration of the biceps reflection
pulley with opaque (left) and transparent capsule and ligaments (right) to demonstrate
the underlying structures. B-D, Coronal FST1 images. E, Axial FST1 MR arthrogram
image. The long head of the biceps tendon (LHBT) is maintained within the bicipital
groove by a complex of static stabilizers including the rotator interval capsule (RIC),
superior glenohumeral ligament (SGHL), coracohumeral ligament (CHL), and
transverse humeral ligament (THL), and dynamic stabilizers including the
supraspinatus tendon (Sup) and subscapularis tendon (Sub). These structures are
collectively referred to as the biceps reflection pulley.
The SA-SD bursa (Figure 6.11) is the largest bursa in the shoulder, which is
most often associated with pathology. It is actually composed of 2 bursae: the
subacromial and subdeltoid; however, they are usually considered as one
structure together because they are usually continuous with each other in around
95% of patients.22 The SA-SD bursa covers a large surface area over the
glenohumeral joint and facilitates movement between the rotator cuff tendons
and the coracoacromial arch and between the rotator cuff tendons and the deltoid
muscle. The bursa is located deep to the acromion and deltoid muscle and
superficial to the rotator cuff muscles and tendons. Its medial margin extends to
the coracoid process and its lateral and inferior margins extend up to 3 cm below
the greater tuberosity of the humerus underlying the deltoid muscle.23 Its
anterior margin extends to cover the bicipital groove.
GLENOHUMERAL INSTABILITY
The glenohumeral joint has a broad range of motion that predisposes it to
inherent instability, making it the most commonly subluxed and dislocated joint
among all peripheral joints.24 Shoulder dislocation can occur secondary to
trauma or in the nontraumatic setting from the underlying morphologic
abnormalities of the static and dynamic stabilizing structures of the joint such as
the glenoid labrum or rotator cuff tendons.25 An acute shoulder dislocation can
occur from a sudden load during a traumatic event such as a fall on an
outstretched arm, which can also be exacerbated with repetition of similar
traumatic episodes. Patients with recurrent shoulder dislocations also often have
recurrent microtrauma in which minor repetitive injuries lead to recurring
shoulder dislocations, which can also lead to injury to the soft-tissue
stabilizers.24,25 Anterior shoulder dislocation is the most common form of
traumatic shoulder instability, accounting for 90% of all dislocation events.26
•
FIGURE 6.10 Normal acromioclavicular joint (ACJ). A, Illustration of the ACJ static
stabilizers with opaque (left) and transparent capsule (right) to demonstrate the
underlying structures. B, Illustration of the ACJ dynamic stabilizers. C, Coronal PD
MR image. D, Coronal fat saturated T2 MR image. E, Sagittal T1 MR image. The
following structures are demonstrated: acromioclavicular joint capsule (ACJC),
clavicle (Clv), acromion (Acr), superior acromioclavicular ligament (SACL), inferior
acromioclavicular ligament (IACL), fibrocartilaginous disk (Disk), coracoclavicular
ligament consisting of the conoid ligament (CL) and trapezoid ligament (TL),
coracoacromial ligament (CAL), deltoid muscle (Del), spine of scapula (S), and
trapezius muscle (Trp). Cor, coracoid.
After a clinically suspected shoulder dislocation, the initial imaging test of

choice is still radiography.24 Cross-sectional imaging with CT and MRI is
commonly used as follow-up imaging studies to further characterize the extent
of injury and for surgical planning.27 CT is typically performed to better
characterize the osseous injuries associated with shoulder dislocation,28,29
whereas MRI and MR arthrography are optimal to evaluate the associated soft-
tissue injuries, such as the labrum and rotator cuff.30
In anterior shoulder dislocation, the mechanism of injury involves anterior-
inferior movement of the humeral head in relation to the glenoid. Anterior
dislocations are usually caused by a direct blow to, or fall on, an outstretched
arm. The patient typically holds the arm in ABER position during the dislocation
event. During dislocation, the IGHL pulls the anterior-inferior margin of the
osseous glenoid rim, which can often result in an avulsion tearing injury of the
labrum referred to as a Bankart labral tear (Figure 6.12), where the labrum and
anterior band of the IGHL are traumatically detached from the glenoid. A more
severe injury can also lead to a fracture of the glenoid with a displaced fracture
fragment, resulting in a bony defect in the glenoid rim referred to as a Bankart
fracture (Figure 6.13). This traumatic glenoid defect or glenoid bone loss is often
described as a cause of an inverted pear–shaped morphology of the glenoid.
Depending on the presence or absence of an osseous fragment, Bankart lesions
are classified as “soft-tissue” or “bony” Bankart.24 In soft-tissue Bankart lesions,
the avulsion mechanism of injury may cause tearing of the labrum and disruption
of its attachment to the glenoid, referred to as the scapular periosteum.
Administration of a contrast agent into the joint space during MR arthrography
may help establish the diagnosis by visualizing extension of contrast beyond the
detachment of the labrum and scapular periosteum. The soft-tissue Bankart
labral tear can be mistaken for a normal variant sublabral foramen or hole;
however, the Bankart labral tear occurs primarily in the anterior-inferior labrum
although it can often extend upward to the anterior superior labrum. In contrast,
a normal variant sublabral foramen is only localized to the anterior superior
labrum. Furthermore, a sublabral foramen should not be associated with a Hill-
Sachs fracture unlike a Bankart labral tear, which usually is. With Bankart
fractures, assessment of the morphology and size of the osseous defect of the
glenoid rim is also essential because substantial glenoid bone loss is associated
with the failure of surgery.6 Anterior shoulder dislocations also often lead to an
impaction fracture deformity of the posterior superior aspect of the humeral head
referred to as a Hill-Sachs fracture. Assessment of the size and morphology of
Hill-Sachs fractures is also important because they are associated with an
increased risk of postoperative recurrence of dislocation.31,32
•
FIGURE 6.11 Normal subacromial-subdeltoid (SA-SD) bursa. Illustration of the SA-
SD bursa with transparent deltoid muscle (left) to demonstrate the underlying
structures and transparent bursa (right) to demonstrate the underlying structures. The
bursa is located deep to the acromion (Acr) and deltoid muscle (Del) and superficial to
the rotator cuff muscles and tendons.
Posterior glenohumeral joint dislocation injuries are much less frequent than
anterior dislocations and are typically associated with seizures as the underlying
causes of the posterior dislocation. Because the forces of injury are reversed, a
reverse Hill-Sachs injury refers to an impaction fracture of the anterior aspect of
the humeral head, and a reverse Bankart injury refers to a fracture and/or tear of
the posterior glenoid and labrum.
LABRAL TEARS
Unstable labral tears are tears that can become displaced and result in clinical
symptoms of pain and impingement for the patient because of the displaced
labral tissue. On physical examination, it can be difficult to determine if a labral
tear is stable or not. During arthroscopy, labral tears can be probed for the
abnormal motion indicative of instability33,34; such tears may require surgical
repair. Tears of the anterior labrum are often the result of traumatic anterior
shoulder dislocation in young patients and are often unstable tears requiring
surgical repair.
Stable labral tears are less likely to become displaced and cause clinical
symptoms and thus often do not require surgical repair and can often be
managed without any surgical intervention if asymptomatic.33,34 Tears of the
superior labrum referred to as SLAP tears, as well as posterior labral tears, are
often nontraumatic or degenerative tears, which can occur in all age groups.
These types of tears are often stable at arthroscopy and may be sometimes
managed conservatively; however, management of these types of tears varies on
a case-by-case basis and may also be treated with surgical repair.35
On coronal MRI, a SLAP tear is present in the superior aspect of the labrum
and is pointing laterally into the labral substance (Figure 6.14). In contrast, a
normal sublabral recess is pointing medially toward the glenoid. MR
arthrography with the administration of a contrast agent into the glenohumeral
joint space is optimal to establish the diagnosis of a labral tear by visualizing
contrast extension beyond the detachment of the labrum. Additional findings
seen with labral tears on MRI include abnormal morphology with fraying or
fragmentation of the labrum, increased signal of the labrum, and displacement of
the torn labral tissue. One study showed a very accurate prediction of unstable
labral tears by using the criterion of a change in the position of the labral tear of
4 mm or more when comparing conventional nonarthrogram MR images with
MR arthrograms.36 Modi et al37 also showed that ABER positioning during MR
arthrography improved accuracy in the diagnosis of labral tears.
•
FIGURE 6.12 Bankart labral tear (BT) and Hill-Sachs (HS) fracture. A, Illustration of
anterior shoulder dislocation with humerus abducted and externally rotated and
dislocated anterior and inferior relative to the glenoid associated with BT and HS
fracture. B and C, Axial FST1 MR arthrogram images after anterior shoulder
dislocation that has been reduced. This injury is associated with a Bankart labral
avulsion tear (BT) of the anterior-inferior labrum that is detached from the glenoid and
an HS fracture of the posterior superior aspect of the humeral head that is affected.
•
FIGURE 6.13 Bankart fracture (BF) and Hill-Sachs (HS) fracture. A, Illustration of
anterior shoulder dislocation with the humerus abducted and externally rotated and
dislocated anterior and inferior relative to the glenoid associated with BF and HS
fracture. B and C, Axial FSPD MR images after anterior shoulder dislocation that has
been reduced. This injury is associated with a BF of the anterior-inferior glenoid with
displaced avulsed glenoid bone fragment and fragmented overlying labrum and an
HS fracture of the posterior superior aspect of the humeral head that is affected.
•
FIGURE 6.14 Superior labrum anteroposterior (SLAP) labral tear. Illustration (A)
and coronal FST1 MR arthrogram image (B) of a SLAP tear of the labrum (arrow)
located mostly between the 11- and 1-o’clock positions along the superior labrum
underlying the biceps-labral complex (arrowhead). On coronal MRI image, the SLAP
tear is present in the superior aspect of the labrum and is pointing laterally into the
labral substance.
ROTATOR CUFF PATHOLOGY

The rotator cuff allows for movement of the arm in space and overhead
activities. It is a frequent source of injury and pain, especially in the aging
population. The rotator cuff muscles have a crucial role in the dynamic
stabilization of the glenohumeral joint. Several studies have demonstrated the
significant negative impact of rotator cuff tears on the dynamic stability of the
shoulder. Specifically, it has been demonstrated that patients with complete
supraspinatus tears that extend into the infraspinatus tendon will likely manifest
significant weakness and altered shoulder kinematics compared with patients
with smaller partial thickness tears.38,39
The spectrum of pathology in the rotator cuff ranges from tendinopathy to
partial- and full-thickness tears (Figure 6.15). The etiology of rotator cuff tears
can be multifactorial. Intrinsic abnormalities include degeneration due to aging,
ischemia, or attrition and extrinsic factors include trauma and impingement.
Rotator cuff impingement is the result of compression of the rotator cuff fibers
by surrounding soft tissue or osseous structures, which are usually related to the
coracoacromial arch from subacromial bone spurs and/or degenerative
osteophytes of the adjacent ACJ, referred to as subacromial impingement.
Posterosuperior internal impingement can also occur in which the posterior
superior humeral head contacts the posterior glenoid during abduction with
external rotation, which is less common than subacromial impingement in the
general population but particularly occurs in throwing athletes.40
Tendinopathy, often also referred to as tendinosis or tendinitis, appears on
MRI as focal or diffuse ill-defined intermediate signal intensity in the tendon
without disruption of tendon articular or bursal surface fibers (Figure 6.16). This
may often also be associated with diffuse or focal tendon thickening.
Tendon tears may involve an articular surface or bursal surface only in which
case they are described as a partial-thickness tear (Figure 6.17) or they may
extend from the articular to bursal surfaces and are thus called a full-thickness
tear (Figure 6.18). Tears can also be confined to the interstitium without articular
or bursal surface extension, referred to as a midsubstance or intrasubstance tear.
On MRI, tendon tears of the rotator cuff appear as focal areas of tendon fiber
disruption with increased signal of fluid-sensitive images, which is of the same
signal intensity as fluid. It is usually best appreciated on fat-suppressed, T2-
weighted sequences. Tears most frequently occur within 1 cm of the insertion
(referred to as the critical zone) or at the humeral head insertion. Tendon tears
are often associated with adjacent tendinopathy.
Full-thickness tears are often classified according to their size into small
(<1 cm), medium (1-3 cm), large (3-5 cm), and massive (>5 cm) tears,13 which
may have implications for the type of surgical repair that is required and
therefore should be routinely assessed on MRI performed to assess the rotator
cuff. The appearance of the tendon margins at the site of a tear should also be
noted, because poor quality tendon fibers around a diffusely torn tendon may not
be suitable for repair. Full-thickness tears and high-grade partial-thickness tears
may often retract, which also has implications for surgical planning and should
be described on MRI. The myotendinous junction of the supraspinatus muscle is
normally located directly above the humeral head, which is referred to as the 12-
o’clock position on coronal MR images with the arm held in neutral position.13
The extent of tendon retraction can be calculated on coronal MR images by
measuring the distance between the greater tuberosity of the humeral head and
the location of the retracted myotendinous junction.
FIGURE 6.15 • Spectrum of rotator cuff pathology. Illustration of rotator cuff

tendinosis with thickening and inflammation of the supraspinatus tendon (arrow);
partial-thickness articular-sided rotator cuff tear in the supraspinatus tendon (arrow);
partial-thickness bursal-sided rotator cuff tear in the supraspinatus tendon (arrow);
full-thickness full-width rotator cuff tear in the supraspinatus tendon (arrow) with
medial retraction of the torn tendon stump (arrowhead).
Calcific tendinitis or tendinosis of the rotator cuff is a self-limiting condition

because of deposition of calcium hydroxyapatite within the rotator cuff tendons,
often associated with calcific bursitis of the overlying SA-SD bursa (Figure
6.19). It is a common presentation of the hydroxyapatite crystal deposition
disease. Patients usually present with acute symptoms of pain, tenderness on
palpation, and swelling or may be entirely asymptomatic. The soft-tissue calcific
deposits are best diagnosed on radiographs where they appear as teardrop shaped
or nodular calcific densities. MRI is often performed to evaluate for any
potential associated inflammation of the surrounding rotator cuff tendons and
SA-SD bursa. On MRI, the calcific depositions appear as teardrop-shaped or
nodular lesions in the bursa and/or rotator cuff tendons, which are hypointense
on T1 and fluid-sensitive (T2FS, PDFS, or STIR) images because of the
calcification. If there is active inflammation associated with the calcific deposits,
there is also often increased fluid and edema along the bursa and tendinosis of
the involved tendon with tendon thickening and increased signal.
SUBACROMIAL-SUBDELTOID BURSA PATHOLOGY

Increased fluid in the SA-SD bursa may be seen in association with rotator cuff
tears, inflammatory disease, crystal deposition disease, and infection. Septic
bursitis infection is not common but is particularly a problem with intravenous
drug users.21 Crystal deposition disease in the SA-SD bursa is referred to as
calcific bursitis and is often associated with calcific tendonitis in the rotator cuff
tendons, usually secondary to hydroxyapatite crystal deposits as described
above.21 Large amorphous tumorallike calcific deposits in the SA-SD bursa may
also be seen in association with chronic renal disease and should also be
considered in the differential diagnosis for calcific bursitis.
FIGURE 6.16 • Rotator cuff tendinosis. Coronal fat saturated T2 MR image
demonstrating supraspinatus tendinosis with intermediately increased signal and
thickening of the tendon (arrow).
•
FIGURE 6.17 Partial-thickness rotator cuff tears. A, Coronal fat saturated T2 (FST2)
MR image of a partial-thickness articular-sided rotator cuff tear in the supraspinatus
tendon (arrow). B, Coronal FST2 MR image of a partial-thickness bursal-sided rotator
cuff tear in the supraspinatus tendon (arrow).
•
FIGURE 6.18 Full-thickness rotator cuff tear. Coronal fat saturated T2 MR image of
a full-thickness rotator cuff tear in the supraspinatus tendon (arrow) with medial
retraction of the torn tendon (arrowhead).
•
FIGURE 6.19 Rotator cuff calcific tendinosis and subacromial-subdeltoid (SA-SD)
bursitis. A, Illustration of the rotator cuff with cross-sectional view of SA-SD bursa. B
and C, Coronal fat saturated T2 MR images with corresponding radiographic view (left
lower inset in B) of rotator cuff calcific tendinosis and bursitis. The calcific deposits
(arrowheads) appear as teardrop-shaped or nodular lesions, which are dense on
radiographs and hypointense on MRI and located in the SA-SD bursa and/or adjacent
rotator cuff tendon. If there is active inflammation associated with the calcific deposit,
MRI will demonstrate tendinosis of the involved tendon with tendon thickening and
increased signal (dashed arrows) and increased fluid and edema along the bursa
secondary to bursitis (solid arrows).
BICEPS TENDON PATHOLOGY

The clinical presentation of injury to the proximal biceps tendon is usually pain
in the anterior aspect of the shoulder associated with loss of forward arm flexion.
Pathology of the LHBT can be divided into 3 categories: impingement
tendinopathy, tendinopathy associated with subluxation, and attrition
tendinopathy.41 Impingement tendinopathy is commonly associated with rotator
cuff tendinopathy resulting from impingement among the humeral head,
acromion, and the CHL during elevation and external rotation of the arm.42,43
Tendinopathy associated with subluxation results from injury to the stabilizing
biceps pulley structures.43 Attrition tendinopathy, which can also be described as
a primary tendinitis,41,44 is the result of local new bone formation along the
greater and lesser tuberosity at the margin of the bicipital groove and adhesions
causing stenosis of the bicipital groove.
Biceps pulley injuries can occur from traumatic or nontraumatic causes.
Traumatic injuries are typically the result of a fall on the outstretched arm in
combination with full external or internal rotation or a backward fall onto the
hand or elbow.45 Nontraumatic injuries are usually due to chronic repetitive
overhand activity, which is typically seen with throwing sports such as baseball,
tennis, and volleyball.46 Biceps pulley injuries may also occur in association
with rotator cuff tears. Tears of the far anterior supraspinatus tendon footprint
insertion and the superior subscapularis footprint insertion at the bicipital groove
(known as anterosuperior rotator cuff tears) may dissect to involve the static
biceps pulley stabilizing structures including the CHL and SGHL.16 Injury to
this area of the rotator cuff can cause instability of the biceps tendon resulting in
biceps tendon subluxation or dislocation from the bicipital groove.46,47
Subluxation or dislocation of the biceps tendon can occur in a medial intra-
articular direction toward the glenohumeral joint or it can take an anterior extra-
articular course, depending on which structures of the biceps reflection pulley
are injured.
Isolated proximal biceps tendon injuries are often treated conservatively with
nonsteroidal anti-inflammatory drugs, physical therapy, and/or steroid injection
into the biceps groove around the biceps tendon. Surgical management is often
necessary if symptoms last >3 months or if there are other injuries associated to
the rotator cuff or labrum.48 In patients with impingement biceps tendinopathy,
surgical subacromial decompression is often performed.43 Direct surgical
therapy for biceps tendon pathology includes shaving of the tendon in mild or
early disease and biceps tenotomy or tenodesis for more advanced disease.44
Biceps tenotomy is the surgical resection of the intra-articular portion of the
biceps tendon. Biceps tenodesis is the surgical resection of the intra-articular
portion of the biceps tendon and reattachment of the distal tendon stump of the
resected tendon to the proximal humeral shaft, which is usually done with a
fixation device such as a screw, anchor, or sutures.
On MRI, the spectrum of biceps tendon pathologic findings includes caliber
changes, contour irregularities, signal intensity abnormalities, partial or complete
tears, and dislocation43,49,50 (Figure 6.20). The intra-articular portion of the
LHBT is optimally visualized on sagittal and coronal MR images, and the extra-
articular portion in the bicipital groove is best seen on axial MR images.43 The
normal biceps tendon on MRI has a diameter range from 2 to 5 mm, has a round
to ovoid morphology, and is homogeneously hypointense on cross-sectional
images.43 Flattening of the tendon, particularly at the entrance to the bicipital
groove, can be a normal finding, which is attributed to the higher forces on the
tendon at this level.43 Increased signal and thickening of the tendon on MRI is
indicative of tendinosis, which is also referred to as tendon degeneration43,49,50
(Figure 6.21).
Partial tears manifest as disruption of a portion of the tendon fibers associated
with attenuation of the tendon, which usually manifests as a longitudinal split
tear where the tendon fibers appear to be split into 2 or more tendon bands17
(Figure 6.22). A complete tear is present when the tendon ruptures and retracts
distally from the bicipital groove resulting in nonvisualization of the tendon43
(Figure 6.23). Dislocation of the tendon occurs when the tendon is dislocated
outside of the bicipital groove, which is usually associated with tearing of the
biceps pulley structures (Figure 6.24). Following biceps tenotomy, MRI will
demonstrate the absence of the intra-articular biceps tendon often with
associated osseous productive changes at the supraglenoid tubercle where the
tendon origin was resected. Following biceps tenodesis, MRI will show the same
findings as biceps tenodesis, in addition to a fixation device (screw, anchor, or
sutures) appearing as foci of magnetic susceptibility artifact at the surgical
reattachment of the distal portion of the resected biceps tendon stump to the
humeral head or the proximal humeral shaft in a subpectoral location.
ACROMIOCLAVICULAR JOINT INJURIES

Injuries of the ACJ account for approximately 10% of all shoulder injuries,
which occur most frequently in the setting of sports and trauma.51,52 Diagnosis
and classification of ACJ injuries are based on a combination of clinical and
conventional radiography52–55 according to the well-established Rockwood
classification56,57 (Figure 6.25), which is crucial for treatment planning. Studies
have shown that MRI may yield additional important findings regarding the
integrity of ligaments that may influence management, and in a considerable
number of patients, the MRI findings may actually change the Rockwood type
determined with radiography.58 Treatment planning is heavily based on the
accurate Rockwood classification of ACJ lesions,51,52,59 which can be difficult
clinically and radiographically. Radiographic evaluation can be challenging
because the ACJ widens not only in traumatic conditions but also with aging as a
normal variant,60 as well as arthroses causing ligamentous laxity, such as
rheumatoid arthritis.61 Furthermore, type II injuries can be difficult to
differentiate from type III injuries on conventional radiography.62,63 The
diagnostic limitations of the standard workup of ACJ injuries with radiography
and clinical evaluation have prompted implementation of MRI for visualization
of ACJ injuries.58,62,64,65 While radiography relies only on joint distance
measurements, MRI also allows direct evaluation of joint-supporting structures,
particularly the static stabilizing ligaments and dynamic stabilizing muscles. An
adapted Rockwood MRI classification has been described by Nemec et al58 in
which injuries to the ligaments (acromioclavicular, coracoclavicular, and
coracoacromial ligaments) and the muscles (trapezoid and deltoid muscles) seen
on MRI are integrated into the Rockwood system (Table 6.1).
Rockwood type I (Figure 6.26) injuries show normal radiographic findings.
MRI shows low-grade sprain/partial tear of the acromioclavicular ligament
and/or low-grade sprain/partial tear of the coracoclavicular ligament.
Rockwood type II (Figure 6.27) injuries demonstrate widening of the ACJ
space, normal or slightly widened coracoclavicular interspace, and 50% superior
clavicular displacement on radiographs. MRI demonstrates complete tear of the
acromioclavicular ligament and/or partial tear of the coracoclavicular and
coracoacromial ligaments.
Rockwood type III (Figure 6.28) injuries exhibit widening of the ACJ space,
increased (25%-100%) coracoclavicular interspace, and 100% superior
clavicular displacement on radiographs. MRI shows complete tear of the
acromioclavicular and coracoclavicular ligaments, detachment of the trapezius
and deltoid muscles from the distal part of the clavicle, and/or additional partial
tear of the coracoacromial ligament.
•
FIGURE 6.20 Spectrum of biceps tendon pathology. Illustration of biceps tendinosis
with thickening and inflammation of the long head of the biceps tendon (LHBT)
(arrow); partial longitudinal split tear of the LHBT with splitting of the extra-articular
portion of the tendon fibers along the bicipital groove and proximal humerus (arrow);
complete rupture of the LHBT with the proximal intra-articular tendon stump located
near the biceps-labral complex (arrow) and retraction of the distal tendon stump to the
level of the proximal humeral shaft (arrowhead) with the absence of the tendon in its
expected location within the bicipital groove (*); medial dislocation of the LHBT out of
the bicipital groove and into the anterior aspect of the glenohumeral joint associated
with tearing of the biceps pulley structures including tears of the superior
glenohumeral ligament (SGHL), coracohumeral ligament (CHL), transverse humeral
ligament (THL), and subscapularis tendon.
•
FIGURE 6.21 Biceps tendinosis. Coronal fat saturated T2 MR image of tendinosis
of the long head of the biceps tendon with tendon thickening and increased signal in
the tendon (arrow).
•
FIGURE 6.22 Biceps tendon split tear. Axial fat saturated T2 MR image of a partial
longitudinal split tear of the long head of the biceps tendon with disruption the extra-
articular portion of the tendon fibers along the proximal humerus associated with
attenuation of the tendon and splitting of the tendon fibers into 2 or more tendon
bands (arrow).
FIGURE 6.23 • Biceps tendon rupture. Axial fat saturated T2 MR image
demonstrating complete rupture of the long head of the biceps tendon with
nonvisualization of the tendon in its expected location within the bicipital groove (*).
FIGURE 6.24 • Biceps tendon dislocation. Axial fat saturated T2 MR image
demonstrating medial dislocation of the long head of the biceps tendon (LHBT) out of
the bicipital groove and into the anterior aspect of the glenohumeral joint. The biceps
pulley structures including the subscapularis tendon (Sub) are completely torn and
therefore not visualized in their expected attachments around the bicipital groove and
are instead replaced by extravasation of joint fluid diffusely along the anterior aspect
of the joint and bicipital groove (arrowheads).
•
FIGURE 6.25 Rockwood classification of acromioclavicular joint (ACJ) separation
injuries. Type I injury is a sprain/partial tear of the acromioclavicular ligament (arrow)
and the ACJ remains anatomically aligned; type II injury is a complete tear of the
acromioclavicular ligament (arrow) and sprain/partial tear of the coracoclavicular
ligaments (arrowheads) with widening of the ACJ space, normal or slightly widened
coracoclavicular interspace, and 50% superior clavicular displacement; type III injury
is a complete tear of the acromioclavicular ligament (arrow) and complete tear of the
coracoclavicular ligaments (arrowheads) with widening of the ACJ space, increased
(25%-100%) coracoclavicular interspace, and 100% superior clavicular displacement;
type IV joint injury is a complete tear of the acromioclavicular ligament (solid arrow),
complete tear of the coracoclavicular ligaments (arrowheads), and complete tear of
the coracoacromial ligament (dashed arrow) with posterior displacement of the distal
clavicle; type V injury is a complete tear of the acromioclavicular ligament (solid
arrow), complete tear of the coracoclavicular ligaments (arrowheads), and complete
tear of the coracoacromial ligament (dashed arrow) with marked superior
displacement of the distal clavicle; type VI injury is a complete tear of the
acromioclavicular ligament (solid arrow), complete tear of the coracoclavicular
ligaments (arrowheads), and complete tear of the coracoacromial ligament (dashed
arrow) associated with inferior displacement of the distal clavicle beneath the coracoid
process. Types III-VI injuries also have detachment of the trapezius and deltoid
muscles from the distal part of the clavicle.
•
FIGURE 6.26 Rockwood type I acromioclavicular joint (ACJ) injury. Coronal fat
saturated T2 MR image shows sprain/partial tear of the acromioclavicular ligament
demonstrated by hyperintense signal edema and fraying of the superior and inferior
acromioclavicular ligaments and joint capsule and bone marrow edema around the
joint (arrow). The ACJ remains anatomically aligned.
Rockwood type IV (Figure 6.29) injuries exhibit posterior displacement of the

distal clavicle on radiographs, which is best appreciated on an axillary view in
which the anterior edge of the distal clavicle is not in line with the anterior
border of the acromion; the acromioclavicular and coracoclavicular distances
may be normal. This injury is a result of a force to the acromion that pushes the
scapula posteriorly. MRI demonstrates rupture of all the 3 ligaments
(acromioclavicular, coracoclavicular, and coracoacromial), as well as
detachment of the trapezius and deltoid muscles from the distal part of the
clavicle. A so-called buttonholing event can occur where the posteriorly
displaced clavicle penetrates the trapezius muscle.62
Rockwood type V injuries can be considered a severe form of type III injury.
On radiographs or MRI, type V injuries demonstrate marked superior
displacement of the distal clavicle just under the skin with visible deformity on
physical examination, and MRI also demonstrates rupture of all the 3 ligaments
(acromioclavicular, coracoclavicular, and coracoacromial) and detachment of the
trapezius and deltoid muscles from the distal part of the clavicle. The unopposed
pull of the sternocleidomastoid muscle results in an increase in the
coracoclavicular distance of 100% to 300%.62
Rockwood type VI injuries are very rare and demonstrate inferior
displacement of the distal clavicle beneath the acromion or coracoid process on
radiographs or MRI, which results from a superior blow to the clavicle. MRI
also demonstrates rupture of all the 3 ligaments (acromioclavicular,
coracoclavicular, and coracoacromial) and detachment of the trapezius and
deltoid muscles from the distal part of the clavicle.
On MRI, the PD-weighted images in the coronal oblique plane are the
optimal imaging parameters to evaluate the ACJ, allowing exact visualization of
acute ligamentous lesions.58,62,64,65 Because the patient is in the supine position
for the MRI study, MRI reduces the amount of gravity-assisted
acromioclavicular displacement that occurs in ACJ injuries, which can result in
markedly different acromioclavicular interspace measurements compared with
those obtained on radiographs.58
Management of ACJ injuries depends primarily on the Rockwood
classification. Rockwood types I and II injuries are treated conservatively (ie,
nonoperatively).66 Types IV-VI injuries require surgical therapy.59,67
Management of type III injuries remains relatively controversial and the choice
of conservative versus operative management is often decided by the orthopedic
surgeon on a case-by-case basis.68,69
Table 6.1 LIGAMENTOUS LESIONS ACCORDING TO ROCKWOOD CLASSIFICATION

ADAPTED FOR MRI
Trapezius
Injury Acromioclavicular Coracoclavicular Coracoacromial and Deltoid
Type Ligament Ligament Ligament Muscles
I Partial tear No tear No tear No tear
I+ Partial tear Partial tear No tear No tear
II− Complete tear No tear No tear No tear
II Complete tear Partial tear No tear No tear
II+ Complete tear Partial tear Partial tear No tear
III Complete tear Complete tear No tear Detachment
from distal
clavicle
III+ Complete tear Complete tear Partial tear Detachment
from distal
clavicle
IV Complete tear Complete tear Complete tear Detachment
from distal
clavicle
V Complete tear Complete tear Complete tear Detachment
from distal
clavicle
VI Complete tear Complete tear Complete tear Detachment
from distal
clavicle
Modified from Nemec U, Oberleitner G, Nemec SF, Gruber M, Weber M,
Czerny C, et al. MRI versus radiography of acromioclavicular joint
dislocation. AJR Am J Roentgenol. 2011;197(4):968–973.
•
FIGURE 6.27 Rockwood type II acromioclavicular joint (ACJ) injury. Coronal fat
saturated T2 (FST2) MR image (A) and sagittal FST2 MR image (B) show a complete
tear of the acromioclavicular ligament (arrow) with nonvisualization of the ligaments,
associated widening of the ACJ space and joint effusion, sprain/partial tear of the
coracoclavicular ligaments with edema and fraying of the ligaments (arrowheads),
and mild superior clavicular displacement. Acr, acromion; Clv, clavicle; Cor, coracoid.
•
FIGURE 6.28 Rockwood type III acromioclavicular joint (ACJ) injury. A and B,
Coronal fat saturated T2 MR images show a complete tear of the acromioclavicular
ligament (arrow) with nonvisualization of the ligaments and surrounding edema,
associated widening of the ACJ space and joint effusion, complete tear of the
coracoclavicular ligaments, which are not visualized (arrowheads), detachment of the
trapezius (Trp) and deltoid (Del) muscles from the distal part of the clavicle (Clv) with
extensive edema around the torn muscle attachments to the clavicle, and superior
displacement of the distal clavicle. Acr, acromion; Cor, coracoid.
•
FIGURE 6.29 Rockwood type IV acromioclavicular joint (ACJ) injury. Coronal fat
saturated T2 (FST2) MR images (A and B) and Sagittal FST2 MR image (C) show a
complete tear of the acromioclavicular ligament (solid arrow) with nonvisualization of
the ligaments and surrounding edema and joint fluid, complete tear of the
coracoclavicular ligaments, which are not visualized (arrowheads), complete tear of
the coracoacromial ligament, which is not visualized and replaced with edema and
fluid (dashed arrow), and associated posterior displacement of the distal clavicle (Clv)
relative to the acromion (Acr). Illustration (D) and coronal PD MR image (E)
demonstrating detachment of the trapezius (Trp) muscle from the distal part of the
clavicle (Clv) and “buttonholing” of the posteriorly displaced clavicle which penetrates
the trapezius muscle (arrow). Cor, coracoid; Del, deltoid.
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2008;39(4):535–545, viii.
1. Which structure passes through the rotator cuff interval of the shoulder?
A. Supraspinatus tendon
B. Subscapularis tendon
C. Coracoid process
D. Middle glenohumeral ligament
2. Which MRI feature is most closely associated with supraspinatus tendinosis?

A. Fluid in the SA-SD bursa
B. Swelling of the supraspinatus tendon
C. Atrophy of the supraspinatus muscle
D. Discontinuity at the musculotendinous junction
3. Which MRI feature of the infraspinatus muscle would be most closely

associated with chronic atrophy?
A. High T2 signal
B. Low T2 signal
C. High T1 signal
D. Low T1 signal
4. Where is the origin of the short head of the biceps tendon?

A. Glenoid process
B. Coracoid process
C. Glenoid labrum
D. Lesser tuberosity

1. C The coracoid process protrudes through the rotator cuff interval.
2. B Tendinosis is associated with swelling and increased T1 and T2 signal.
3. C Chronic atrophy results in fatty replacement of muscle, which has high T1
signal.
4. B The short head of the biceps tendon originates at the coracoid process. The
long head originates at the glenoid process.
7
MRI of Elbow Injuries
Hyojeong Mulcahy
This chapter covers MRI techniques, anatomy, and findings of injuries of the
elbow.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of MRI of elbow injuries, the learner will be able to
4. summarize relevant concepts and knowledge for the following topics: anatomic variants and
pitfalls, cartilage and bone injury, ligament injury, myotendinous injury, and nerve entrapment or
injury.
IMAGING TECHNIQUE
Generally, the elbow may be scanned with the patient in supine position with the
arm at the side, elbow extended, and forearm supinated.1,2 A dedicated
circumferential elbow coil can be used in this position. The larger phased array
coil is preferred for examination of larger areas. Alternatively, the patient may
assume a prone position with the arm above the head and the elbow extended
(Superman position). The elbow should be scanned from 10 cm above the joint
to bicipital tuberosity, distally. In our institution, sagittal proton density (PD),
axial and coronal T1, and T2 fat-saturated (FS) sequences are obtained for
routine elbow MRI. For MR arthrography, axial T1, axial T2 FS, coronal T1 FS,
coronal T2 FS, and sagittal T2 FS sequences are obtained after injecting the
elbow joint with a gadolinium-based contrast mixture. The flexed abducted
supinated view protocol is used for imaging of distal biceps tendon, in which the
patient lays prone with the shoulder abducted 180° and the arm beside the head.
The elbow is flexed to 90°, with the forearm supinated, thumb up, and a shoulder
phased array coil placed around the elbow.3
DICTATION CHECKLIST
Our dictation checklist for elbow MRI includes bones and bone marrow, joint
alignment, articular cartilage, medial and lateral collateral ligaments, common
flexor and common extensor tendons, biceps and brachialis tendons, triceps
tendon, muscles, joint fluid and synovium, bursal fluid, vessels and nerves, focal
lesions, cysts and masses, and subcutaneous tissues. Each of these sets of
structures should be identified and evaluated for morphology and signal
OSSEOUS AND ARTICULAR ANATOMY

The elbow is a compound trochoginglymoid joint formed by the articulations of
the humerus, ulna, and radius.4 The ulnohumeral articulation is a hinge
(glymoid) joint, whereas the radiohumeral and radioulnar articulations are pivot
(trochoid) joints.
The proximal aspect of the elbow joint is formed by the humerus with 2
central condyles that comprise the articular surfaces of the humerus and 2
peripheral epicondyles that serve as attachment sites for soft-tissue structures.
The articular surface of the distal humerus is divided into the trochlea and the
capitellum, which articulate with the ulna and radius, respectively. The radial
head also articulates with the adjacent radial notch of the ulna. This allows the
radial head to rotate, providing supination and pronation of the forearm. The
capitellum and trochlea have smooth surfaces lined by articular cartilage, and the
epicondyles are extra-articular structures with a rough, irregular contour. The
trochlear notch of the olecranon surrounds almost 180° of the trochlea, making
the ulnohumeral articulation as the most important stabilizer of the elbow under
varus stress. The remainder of the stabilization is provided by the
capsuloligamentous structures.
The articular capsule of the elbow is thin anteriorly and posteriorly.
Additional support is provided anteriorly by the brachialis muscle and
posteriorly by the triceps muscle. Medially and laterally, the capsule blends with
the medial and lateral collateral ligaments. Five main synovial recesses can be
distinguished within the elbow. The olecranon recess is the largest of the five.
The anterior humeral recess is divided into the coronoid and radial fossae. The
annular recess surrounds the radial neck. The ulnar collateral ligament (UCL)
and radial collateral ligament (RCL) recesses are deep in the respective UCL and
RCL. Synovial folds of various sizes and shapes normally project into the joint
space and should not be mistaken for intra-articular loose bodies. Three major
fat pads are situated intra-articular but extrasynovial. Two anterior fat pads
correspond to the capitellar and trochlear fossae, whereas a single posterior fat
pad is concealed within the olecranon fossa. Therefore, in the presence of a joint
effusion confined by the synovial capsule, the extrasynovial fat pads are
elevated, resulting in the radiographic signs of visible posterior and anterior fat
pads (Figure 7.1).
•
FIGURE 7.1 Fat pad sign. Lateral radiograph of the elbow in a patient with a radial
neck fracture (black arrow) shows anterior (white arrow) and posterior (white
arrowhead) fat pads.
LIGAMENTS
The collateral ligament complexes provide supplementary support for the elbow
medially and laterally.5 The UCL originates from the inferior aspect of the
medial epicondyle, and the lateral collateral ligamentous (LCL) complex arises
from the lateral epicondyle. These collateral ligament complexes are best
demonstrated on coronal images. Axial and sagittal images are useful to confirm
suspected pathology. Ligaments are generally uniformly low in signal on all
pulse sequences.
The UCL is much stronger than the LCL complex. The UCL is comprised of
3 bands that are in continuity with each other: the anterior, posterior, and
transverse bands. The anterior band is the dominant structure and the primary
constraint resisting valgus stress on the elbow. It originates from the inferior
margin of the medial epicondyle and inserts at the sublime tubercle of the
proximal ulna (Figure 7.2A). The posterior band is smaller and has a fanlike
configuration. It originates from the inferior aspect of the medial epicondyle and
inserts at the posteromedial margin of the trochlear notch, forming the floor of
the cubital tunnel (Figure 7.2B). The transverse band plays little if any functional
role and is not readily visualized on routine MRI.
The LCL complex consists of the RCL, lateral ulnar collateral ligament
(LUCL), and the annular ligament. A fourth component, the accessory lateral
collateral ligament, is variably present, extending from the annular ligament to
the supinator crest. The LUCL and RCL may appear contiguous at their origin
on the lateral epicondyle. The RCL inserts broadly on the annular ligament,
whereas the LUCL passes along the posterolateral margin of the radial head
where it blends with fibers of the annular ligament and continues medially to
insert on the supinator crest of the ulna (Figure 7.3). The LUCL is the primary
stabilizer against varus stress, and its disruption can lead to posterolateral
rotatory instability of the elbow. The annular ligament originates from the
anterior and posterior margins of the radial notch, encircling the radial head and
acting as the primary stabilizer of the proximal radioulnar joint (Figure 7.4).
•
FIGURE 7.2 Normal ulnar collateral ligament (UCL) (different patients). A, Coronal
T2 FS MR arthrography. B, Axial T1 MRI. The anterior band of UCL (arrows in A). The
posterior band forms the floor of the cubital tunnel (arrows in B). CFT, common flexor
tendon. Ulnar nerve (arrowhead) in the cubital tunnel.
MUSCLES AND TENDONS

Generally, there are 4 basic movements in the elbow and forearm. The elbow is
limited to flexion and extension. Pronation and supination occurs between the
radius and ulna. Muscles of the elbow are divided into anterior, posterior,
medial, and lateral groups.
•
FIGURE 7.3 Normal lateral collateral ligament complex (different patients). A,
Coronal T2 FS MR arthrography. B, More posterior image. The lateral ulnar collateral
ligament (LUCL) and radial collateral ligament (RCL) may appear contiguous at their
origin on the lateral epicondyle. The RCL inserts broadly on annular ligament (arrows
in A). The LUCL passes along the posterolateral margin of the radial head to insert on
the supinator crest of the ulna (arrows in B). CET, common extensor tendon.
•
FIGURE 7.4 Normal annular ligament and recess on axial T2 FS MR arthrography
(arrows).
The medial muscle group includes the pronator teres and 4 superficial
common flexors: the flexor carpi radialis, palmaris longus, flexor carpi ulnaris,
and flexor digitorum superficialis. The common flexor muscles at the level of
the elbow form a confluent muscular mass at the posteromedial aspect of the
joint. On coronal MRI, the common flexor tendon appears as a hypointense band
that gradually blends with proximal fibers of the UCL arising from the
undersurface of the medial epicondyle (Figure 7.2).1–4
The lateral muscle group consists of 3 components: a superficial group, the
common extensors, and the supinator. The common extensor group is composed
of 4 muscles: the extensor carpi radialis brevis (ECRB), extensor digitorum,
extensor digiti minimi, and extensor carpi ulnaris. The common extensor tendon
is visualized on coronal MRI as a hypointense band arising from the lateral
epicondyle, and the common extensors are found along the posterolateral aspect
of the elbow, blending with the more substantial superficial muscle (Figure 7.3).
The ECRB and LCL complex are closely applied to each other and may not be
differentiated on MRI.
The anterior muscle group includes the 2 primary flexors of the elbow, the
biceps brachii and brachialis. Axial images generally provide the best
visualization of the biceps and brachialis, as they insert on the radial tuberosity
and onto the proximal ulna near the coronoid process, respectively.
The posterior muscle group includes the 2 primary extensors of the elbow, the
anconeus and triceps. Sagittal images provide the best visualization of the triceps
insertion to the olecranon process. The anconeus arises from the posterior lateral
epicondyle and inserts onto the lateral ulna, and axial images provide the best
visualization.
BURSAE
There are several superficial and deep bursae about the elbow that should be
emphasized because of the potential for confusion with cysts or other pathology
on MRI, the most important of which are the olecranon and the cubital bursae.
The superficial olecranon bursa is seen most commonly and is found in the
subcutaneous tissue dorsal to the olecranon (Figure 7.5). The other 2 superficial
bursae, the medial epicondylar and lateral epicondylar, should not be confused
with disruptions or tears in the medial and lateral collateral ligaments. The
cubital bursae include the bicipitoradial and the interosseous bursae. The
bicipitoradial bursa covers the anterior aspect of the radial tuberosity and is
intimately associated with the insertion of the biceps brachii. An inflamed bursa
can be differentiated from a simple effusion by the lack of fluid in the anterior
compartment of the elbow. These bursae are normally not identified, but when
inflamed and fluid-filled (because of direct acute trauma, chronic repetitive
stress, infection, and various inflammatory disorders, such as gout and
rheumatoid arthritis), they can be demonstrated on T2-weighted or GRE images
(Figure 7.6).
•
FIGURE 7.5 Olecranon bursitis (arrow) on axial T2 FS MRI. R, radius; U, ulna.
ANATOMIC VARIANTS AND PITFALLS

Pitfalls in interpreting MRI of the elbow are usually related to normal anatomic
variants, technical errors, patient motion, and various imaging artifacts.4–6
A frequent osseous variant is the supracondylar process. This hooklike, bony
projection is a vestigial remnant that is also seen in birds and is present in up to
2.7% of humans (Figure 7.7). This structure is almost always asymptomatic.
However, a ligamentous structure (ligament of Struthers) can extend from the
supracondylar process to the medial epicondyle, forming an osteofibrous tunnel
over the median nerve, and can be associated with compression neuropathy.
Identification of the supracondylar process is easily accomplished with routine
radiography. However, the relationship of the ligament of Struthers to the
neurovascular structures may be most easily viewed with coronal and axial MRI.
At the posterior junction of the capitellum and the distal humerus, there is a
groove where the articular surface ends that may appear as a pseudodefect on
sagittal MRI (Figure 7.8), simulating an osteochondral lesion. Osteochondral
lesions, Panner disease, and even geodes from arthritis tend to be anterior, not
posterior. Also, true osteochondral lesions are typically associated with
additional evidence of injury, such as marrow edema. Although posterior
capitellum impaction injuries may occur, they are uncommon.
•
FIGURE 7.6 Bicipitoradial bursitis. A, Axial T2 FS MRI. B, Sagittal T1 FS Gd MRI.
The bursa appears as a homogeneous, high-intensity structure with clearly defined
margins (black arrows in B). The bursa surrounds the distal biceps tendon (white
arrows).
In the ulna, the trochlear notch has a figure-of-eight configuration with slight
constriction midway between the coronoid and olecranon processes, traversed by
a slight bony elevation called the trochlear ridge. It is 1 to 2 mm wide and
usually has the same height, or it is just higher than the adjacent hyaline cartilage
(Figure 7.9). This anatomic structure may simulate either a central osteophyte or
an olecranon stress fracture. The peripheral constriction of the trochlear notch
results in peripheral medial and lateral pseudodefects with cortical interruption
in the articular surface, which should not be misinterpreted as an osteochondral
lesion.
•
FIGURE 7.7 Supracondylar process (arrow) on lateral elbow radiograph. It extends
from the distal anteromedial humeral cortex and should not be mistaken for an
osteochondroma.
FIGURE 7.8 • A pseudodefect of capitellum (arrow) on sagittal T2 FS MR
arthrography. It is identified as a notch, deeper laterally, easily identified in sagittal
images but also seen in the coronal plane.
•
FIGURE 7.9 Trochlear ridge of ulna (arrow) on sagittal T1 MR arthrography. MRI
reveals a central elevation of the trochlear articular surface corresponding to the
trochlear ridge.
The elbow has synovial folds or synovial plicae that are embryologic
remnants. The synovial folds have typical synovial membrane histology, with
occasional polypoid projections, and are low in signal on all MR sequences.
Synovial folds or synovial fringes are most frequently seen at the lateral aspect
of the joint, but also may occur at the superior margin of the lateral olecranon
recess (Figure 7.10). These are usually asymptomatic, although repetitive injury
may create an inflammatory reaction. Possible symptoms of a symptomatic plica
include pain, joint locking, and snapping, simulating an intra-articular body, the
so-called plica syndrome.
The anconeus epitrochlearis is an anomalous muscle, sometimes considered
an accessory to the medial head of the triceps, and is present in 3% to 28% of
cadaver elbows (Figure 7.11). Even though considered a variant, this accessory
muscle, such as those seen in the tarsal tunnel of the foot, may cause ulnar
neuropathy.
CARTILAGINOUS AND OSSEOUS INJURY

Little Leaguer’s elbow, also known as medial epicondyle apophysitis, refers to a
medial-sided elbow injury that occurs in skeletally immature baseball pitchers.7
Repeated valgus stress causes traction injury to the apophysis of the medial
epicondyle of the humerus. Radiographs may show physeal widening. On MRI,
fluid-sensitive sequences show edema adjacent to the apophysis (Figure 7.12).
•
FIGURE 7.10 Synovial folds. A, Coronal T1 FS MR arthrography shows a lateral
synovial fold/fringe (arrow). B, Axial T1 MR arthrography shows a posterosuperior
synovial fold in olecranon recess (arrow).
FIGURE 7.11 • Anconeus epitrochlearis. Axial T1 MRI shows the anconeus
epitrochlearis (short white arrows) near the normal ulnar nerve (long black arrow).
The anconeus epitrochlearis arises from the medial humeral condyle, passes
superficial to the ulnar nerve in the cubital tunnel, and inserts on the olecranon.
Panner disease refers to a lateral-sided elbow injury that also occurs in

skeletally immature throwers. Repeated valgus stress causes chronic
compression at the unfused capitellar epiphysis. Radiographs may show lucency
in the capitellum. On MRI, fluid-sensitive sequences show edema in the marrow
surrounding the capitellar epiphysis without a chondral defect. Both Little
Leaguer’s elbow and Panner disease occur most commonly in 9 to 12 year olds,
and patients present with pain that is relieved by rest. Generally, patients do well
with conservative treatment.
Osteochondral disease (OCD) is also a lateral-sided elbow injury related to
chronic compression. It tends to occur in slightly older throwers, most
commonly adolescent male baseball pitchers aged 10 to 16 years. Patients may
report diffuse elbow pain and mechanical symptoms, such as catching and
locking. MR findings include flattening of the subchondral bone, bone
fragmentation, chondral defects, and subchondral marrow edema on fluid-
sensitive sequences (Figure 7.13). Signs of instability include fluid signal around
a bone fragment or a free fragment. Intra-articular contrast extension deep to the
fragment implies an unstable lesion, on MR arthrography. Patients with unstable
lesions require surgery. Although OCD lesions occur in the capitellum in most
cases, they may rarely occur at other articular surfaces, such as the humeral
trochlea or radial head.
Olecranon stress injuries are associated with upper limb–dominated sports,
such as baseball, tennis, weightlifting, and gymnastics. In the setting of stress
reaction, fluid-sensitive MRI demonstrates marrow edema. In stress fracture, an
irregular T1 hypointense line is present, surrounded by abnormal marrow signal
(Figure 7.14).
Loose body formation can complicate many of these disorders and may even
result from osteophyte fracture. Loose bodies can accelerate degenerative
changes and are often removed surgically. GRE MRI or MR arthrography can
improve detection.
LIGAMENT INJURY
In the medial elbow, the UCL is the main stabilizer against valgus stress.
Rupture of this ligament is a catastrophic injury to the athlete. Most commonly
the tears result from chronic repetitive trauma, as seen in activities such as
baseball pitching and javelin throwing.8,9 Acute traumatic injury occurs usually
after a fall on the outstretched arm. The majority of UCL complex tears involve
the anterior band, and most tears are complete and involve the midsubstance of
the ligament (Figure 7.15). Partial tears of the anterior band of the UCL complex
most commonly occur along the humeral attachment in baseball pitchers. On
MRI, UCL tears are diagnosed by an area of discontinuity, laxity of the ligament,
irregularity, poor definition, and increased signal intensity within and adjacent to
the ligament on fluid-sensitive sequences. MR arthrography is much more
accurate compared with conventional MRI for detection of partial tears. Partial
tears of the articular surface of the anterior band of the UCL near the sublime
tubercle may demonstrate a T-sign (Figure 7.16). In chronic tears, heterotopic
ossification may be present, and accompanying radiographs may be useful for
diagnosis.
FIGURE 7.12 • Medial apophysitis in a 13-year-old baseball pitcher. A,
Anteroposterior radiograph. B, Coronal T1 MRI. C, Coronal T2 FS MRI. A radiograph
of the elbow shows a widening of the physis of medial epicondyle. Coronal MRI
demonstrates edema around the medial epicondyle, physeal widening and irregularity,
and mild displacement of epiphysis.
•
FIGURE 7.13 Osteochondral disease (OCD) in the capitellum in a 14-year-old
gymnast. A, Anteroposterior radiograph. B, Coronal T1 MR arthrography. C, Sagittal
T2 FS MR arthrography. OCD in the capitellum is seen as a subchondral lucency on a
radiograph. MR arthrography demonstrates subchondral flattening, edema, and cysts.
There is no evidence of contrast invagination to suggest instability.
Injury to LCL complex is less common and usually is the result of varus
stress. LCL complex injury is an important entity that can lead to posterolateral
rotatory instability of the elbow. The LUCL most often tears proximally.
Because the RCL and LUCL share a common origin, injury often involves both
structures (Figure 7.17). The same MRI approaches described with UCL imaging
can be used for LCL complex evaluation. Sagittal images may show posterior
subluxation of the radial head relative to the capitellum.
MUSCLE AND TENDON INJURY
Lateral epicondylitis (tennis elbow) is the most common tendon pathology
encountered in the elbow.10 It is a chronic overuse injury of common extensor
tendon at its origin on the lateral epicondyle resulting from repetitive
microtrauma. The primary site of involvement is the ECRB (Figure 7.18).
Medial epicondylitis (golfer’s elbow) represents injury to the flexor-pronator
muscle group at its origin on the medial epicondyle of the humerus (Figure
7.19). It occurs much less commonly than lateral epicondylitis. The chronic
overuse pattern predominantly affects the flexor carpi radialis and pronator teres
muscles. In tendinopathy, MRI demonstrates thickening and intermediate signal
in the tendon. Partial tears will show thinning or partial disruption of the tendon
and an increased signal on fluid-sensitive MR sequences. Complete rupture of
the tendons will lead to a tendinous gap containing fluid signal and distal
retraction of the involved muscles. Current therapies for lateral and medial
epicondylitis include activity restriction and immobilization. Newer therapies
have shown encouraging results and include injections of autologous blood or
platelet-rich plasma.
•
FIGURE 7.14 Stress fracture of olecranon process. Sagittal T2 FS MR arthrography
shows a linear transverse stress fracture with fluid signal at the olecranon process
(arrow).
•
FIGURE 7.15 Complete tear of anterior band of ulnar collateral ligament (UCL).
Coronal T2 FS MR arthrography shows complete tear of UCL associated with intra-
articular contrast extravasation (arrow).
FIGURE 7.16 • Partial tear of ulnar collateral ligament. Coronal T2 FS MR
arthrography shows the intra-articular contrast extending distally from the joint line
along the cortical margin of the sublime tubercle (arrow) that is referred as “T-sign.”
•
FIGURE 7.17 Complete tear of the lateral ulnar collateral ligament (LUCL) complex.
Coronal T2 FS MR arthrography shows a complete tear at the proximal common
origin of the LUCL complex (arrow) associated with a partial tear of common extensor
tendon.
Most biceps tendon ruptures involve the proximal tendon at the shoulder
(90%-97%), and complete tears of the distal biceps tendon at the elbow account
for only 3% to 5% of biceps injuries. Although relatively rare in the young
athletes, distal biceps tendon rupture can occur in football players and
weightlifters, at or near its insertion onto the radial tuberosity as a result of
forced hyperextension with the arm flexed and supinated. MRI is helpful to
discriminate between partial- and full-thickness tears, estimate the amount of
tendon retraction, and evaluate the integrity of the bicipital aponeurosis (also
known as “lacertus fibrosus”) (Figure 7.20). Triceps tendon rupture is rare in
athletes. Common mechanisms include falling on an outstretched hand, trauma
from a direct blow, and forced flexion during active extension. Tears most
commonly occur distally at the olecranon insertion and may be accompanied by
a small avulsion fracture. Partial tears typically affect the central third of the
tendon distally (Figure 7.21). The normal broad and striated appearance of the
distal triceps tendon should not be misinterpreted as pathologic.
•
FIGURE 7.18 Lateral epicondylitis. Coronal T2 FS MR arthrography shows a partial
thickness tear of common extensor tendon at lateral epicondyle mainly involving
extensor carpi radialis brevis (arrow).
•
FIGURE 7.19 Medial epicondylitis. Coronal T2 FS MR arthrography shows a partial
thickness tear of common flexor tendon at medial epicondyle (arrow).
•
FIGURE 7.20 Distal biceps tendon tear. A, Axial T2 FS MRI at radial insertion. B,
More proximal image. There is fluid in the antecubital fossa with marrow edema at
empty radial tuberosity (arrow in A). Proximal retraction is demonstrated (arrow in B)
when there is associated tearing of the bicipital aponeurosis (arrowhead in B). Partial
tears may demonstrate fluid signal in the tendon substance or peritendinous edema.
•
FIGURE 7.21 Distal triceps tendon tear. Sagittal T2 FS MRI shows partial thickness
tear at distal triceps near olecranon insertion (white arrow). The tear involves central
and posterior fibers. There is an associated full-thickness tear of distal biceps tendon
retracted at the level of distal humerus (black arrow).
•
FIGURE 7.22 Ulnar neuritis at cubital tunnel. A, Axial T1 MRI shows obliteration of
surrounding fat by hypertrophy of the nerve in the cubital tunnel (arrow). B, Axial T2
FS MRI shows increased signal in the ulnar nerve (arrow).
NERVE ENTRAPMENT OR INJURY

The ulnar nerve is most frequently injured at the elbow as it passes through the
cubital tunnel. Cubital tunnel syndrome refers to the clinical manifestations of
ulnar nerve compression, which may occur in the setting of osteophytes,
thickening of the retinaculum, UCL thickening, muscle hypertrophy, or an
anomalous accessory muscle called the anconeus epitrochlearis. In some
patients, the cubital tunnel retinaculum is absent, allowing for subluxation or
dislocation of the ulnar nerve over the medial epicondyle, which can result in
friction neuritis. Evaluation of the ulnar nerve is most easily accomplished using
axial MRI.11 On fluid-sensitive sequences, the inflamed ulnar nerve is bright and
enlarged (Figure 7.22). Signal intensity changes have been described in up to
60% of asymptomatic patients, and the diagnosis of ulnar neuritis should be
made cautiously when there is no enlargement of the nerve.
Posterior interosseous nerve syndrome is a motor neuropathy related to
extrinsic compression. The radial nerve branches into the posterior interosseous
and superficial radial nerves, and compression of the posterior interosseous
nerve may occur where it plunges into the proximal supinator muscle belly at the
elbow. Causes of compression include fibrous bands at the radial head,
prominent radial vessels, a distended bicipitoradial bursa, a prominent edge of
the ECRB, and the proximal edge of the supinator muscle (known as the “arcade
of Frohse”). The site of compression may not be detectable with imaging. On
MRI, the typical pattern of denervation edema or atrophy in the supinator muscle
and extensor muscle group is observed (Figure 7.23). Direct visualization of the
median and radial nerves at the elbow is typically limited.
•
FIGURE 7.23 Posterior interosseous nerve syndrome. Axial T1 MRI demonstrates
fatty atrophy of supinator muscle (arrow).
References
1. Berquist TH. MRI of the Musculoskeletal System. 6th ed. Philadelphia: Lippincott Williams & Wilkins;
2012.
2. Chung CB, Steinbach LS, eds. MRI of the Upper Extremity: Shoulder, Elbow, Wrist, and Hand.
Philadelphia: Wolters Kluwer Health; 2010.
3. Giuffrè BM, Moss MJ. Optimal positioning for MRI of the distal biceps brachii tendon: flexed abducted
supinated view. AJR Am J Roentgenol. 2004;182(4):944–946 [PMID:15039168].
4. Fowler KA, Chung CB. Normal MR imaging anatomy of the elbow. Radiol Clin North Am.
2006;44:553–567, viii.
5. Husarik DB, Saupe N, Pfirrmann CW, et al. Ligaments and plicae of the elbow: normal MR imaging
variability in 60 asymptomatic subjects. Radiology. 2010;257:185–194.
6. Sampaio ML, Schweitzer ME. Elbow magnetic resonance imaging variants and pitfalls. Magn Reson
Imaging Clin N Am. 2010;18:633–642.
7. Iyer RS, Thapa MM, Khanna PC, Chew FS. Pediatric bone imaging: imaging elbow trauma in children
—a review of acute and chronic injuries. AJR Am J Roentgenol. 2012;198(5):1053–1068.
doi:10.2214/AJR.10.7314 [PMID:22528894].
8. Wong TT, Lin DJ, Ayyala RS, Kazam JK. Elbow injuries in adult overhead athletes. AJR Am J
Roentgenol. 2017;208(3):W110–W120. doi:10.2214/AJR.16.16511 [Epub January 17, 2017.
PMID:28095019].
9. Wenzke DR. MR imaging of the elbow in the injured athlete. Radiol Clin North Am. 2013;51:195–213.
10. Donaldson O, Vannet N, Gosens T, Kulkarni R. Tendinopathies around the elbow part 2: medial elbow,
distal biceps and triceps tendinopathies. Shoulder Elbow. 2014;6(1):47–56. doi:10.1111/sae.12022
[Epub June 10, 2013. PMID:27582910; PMCID:PMC4986646].
11. Miller TT, Reinus WR. Nerve entrapment syndromes of the elbow, forearm, and wrist. AJR Am J
Roentgenol. 2010;195(3):585–594. doi:10.2214/AJR.10.4817 [PMID:20729434].
1. Which elbow structure is most commonly injured by valgus stress?

A. Lateral ulnar collateral ligament
B. Anterior band of the ulnar collateral ligament
C. Common extensor tendon
D. Common flexor tendon
2. Which radiologic feature is characteristic of common extensor tendonitis?

A. T-sign on MR arthrography
B. Low signal on T1 MRI
C. High signal on PD FS MRI
D. High attenuation on CT
3. Which elbow tendon is found on MRI to be most frequently injured?

A. Biceps
B. Triceps
C. Common flexor
D. Common extensor
4. Anatomically, the ulnar nerve is most closely associated with which elbow
structure?
A. Lateral epicondyle
B. Brachialis tendon
C. Ulnar collateral ligament
D. Common extensor tendon
1. B The anterior band of the ulnar collateral ligament is the primary static
stabilizer against valgus elbow stress.
2. C Common extensor tendinitis should show increased T1 and T2 signal; the
high T2 signal will be evident on PD FS MRI.
3. D Common extensor tendon injuries (tennis elbow) are the most frequently
found tendon injuries on elbow MRI.
4. C At the elbow, the ulnar nerve passes through the cubital tunnel. The
posterior band of the ulnar collateral ligament forms the floor of the cubital
tunnel.
8
MRI of Hip Injuries
Radiography and CT are the primary imaging modalities used in patients with
acute trauma. An anteroposterior pelvis radiograph is part of our standard trauma
protocol, and the pelvis is included when CT is indicated in these patients. For
patients sustaining low-energy trauma or chronic activity-related injuries, MRI
may be more appropriate than CT if radiographs do not provide the diagnosis.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of MRI of hip injuries, the learner will be able to
4. summarize relevant concepts and knowledge for the following topics: proximal femur injuries,
osteonecrosis, transient bone marrow edema syndrome, myotendinous injuries, athletic
pubalgia, acetabular labral injuries, femoroacetabular impingement, postarthroplasty hip pain,
and miscellaneous hip conditions.
MRI TECHNIQUES
Clinical evaluation of hip and pelvic pain may not localize the source of
symptoms, and nonspecific clinical descriptions such as groin pain, hip pain, and
pelvic pain are common. At Brigham and Women’s Hospital, our current routine
MRI pelvis protocol includes coronal STIR, coronal T1, axial PD, axial T2 FS,
and sagittal T2 FS of the entire pelvis. If there is concern of an abnormality
specific to the hip, we perform our MRI hip protocol, which includes coronal
STIR and coronal T1 of the entire pelvis followed by axial PD, axial T2 FS,
coronal PD, coronal PD FS, and sagittal PD FS of the symptomatic hip. If the
MRI is performed to evaluate for a questioned mass or known neoplasm, we
perform our MRI pelvis tumor protocol, which includes coronal STIR, coronal
T1, axial PD, and 3D axial T1 FS before the administration of intravenous
gadolinium and sagittal T2 FS, 3D axial T1 FS, and coronal T1 FS after the
administration of intravenous gadolinium.
For patients in whom an acetabular labral tear is suspected, we recommend
MR arthrography of the hip at Brigham and Women’s Hospital. To improve
visualization of the labrum and cartilage, we perform our MR arthrograms on a
3 T-field strength magnet. Our protocol includes axial T2 FS, axial T1 FS,
coronal T1 FS, coronal PD, and sagittal T1 FS. We also include a radial T1 FS
sequence to optimize the evaluation of the labrum and articular cartilage.1
Elderly patients may present to the emergency department with hip pain after
ground level falls or other low-energy trauma. If the radiographs are negative for
a fracture and the clinical evaluation remains suspicious for a fracture, further
evaluation with MRI is usually recommended. At Brigham and Women’s
Hospital, we perform our occult fracture pelvis MRI protocol, which includes
coronal T1, coronal STIR, and axial T2 FS through the entire pelvis.
DICTATION CHECKLIST
Our dictation checklist for pelvis-hips MRI includes bones and bone marrow,
joint alignment, articular cartilage, acetabular labrum, tendons and tendon
sheaths, muscles, joint and bursal fluid, sciatic nerve, femoral neurovascular
bundle, focal lesions, cysts and masses, and subcutaneous tissues. Each of these
sets of structures should be identified and evaluated for morphology and signal
characteristics. Any region of high T2 signal should attract further scrutiny.
Specific comments are usually made concerning fracture, osteonecrosis, and
arthritis of hip and sacroiliac joints. The visceral anatomy should be scanned for
significant abnormalities. The clinical indication should be specifically
addressed.
ANATOMY
The bony hip, a ball-and-socket joint, is composed of the proximal femur and
acetabulum. The acetabulum is formed by the fusion of the ilium, pubis, and
ischium, which are separated by the triradiate cartilage in children. The proximal
femur is composed of the femoral head, femoral neck, greater trochanter, and
lesser trochanter. The trochanters are apophyses at the junction of the femoral
neck and shaft and add mass and width to the proximal femur. The greater
trochanter arises from the lateral aspect of the proximal femur, projects
superiorly, and provides attachment to the gluteus medius, gluteus minimus,
piriformis, and obturator internus muscles. The lesser trochanter projects
medially from the posteromedial aspect of the proximal femur and is the
insertion site of the iliopsoas tendon.
Multiple muscle groups at the hip joint allow for a wide range of motions
(Figure 8.1). Medial muscles of the hip include the adductor magnus, adductor
longus, adductor brevis, pectineus, and gracilis, which predominately adduct the
hip, and the obturator externus muscle, which laterally rotates the hip. Posterior
muscles of the hip (hamstrings) include the biceps femoris, semimembranosus,
and semitendinosus, which extend the hip and flex the knee. Anterior muscles of
the hip include the sartorius, rectus femoris, and iliopsoas, which flex the hip.
The muscles of the gluteal region include the gluteus maximus, gluteus medius,
gluteus minimus, tensor fascia lata, piriformis, obturator internus, superior and
inferior gemelli, and quadratus femoris muscles. The gluteus maximus extends
the hip. The gluteus minimus and medius abduct medially rotate the hip. The
piriformis, obturator internus, gemelli, and quadratus femoris muscles laterally
rotate the hip.
The acetabular labrum is a fibrocartilaginous structure apposed to the bony
acetabular rim. Similar to the glenoid labrum, it deepens the acetabulum. The
labrum covers the anterior, superior, and posterior portions of the acetabular rim;
the deficient inferior portion is connected by a transverse ligament. The labrum
has a triangular cross section and normally has uniformly dark signal on T1, PD,
and T2 MRI, similar to the glenoid labrum or the menisci of the knee (Figure
8.2). The locations about the acetabular labrum may be specified using a clock
position, where 12 o’clock is superior and 9 o’clock is anterior. A sublabral
recess is a normal anatomic variant, where the base of the labrum connects with
the articular cartilage, an anatomic situation similar to the shoulder. Sublabral
recesses are characteristically found at the posterior labrum as well as anteriorly
in the 8-o’clock position (Figure 8.3).2,3
The sciatic nerve needs to be carefully evaluated, as it can be injured after
trauma or hip arthroplasty. Abnormal masses along the course of the sciatic
nerve or compression of the sciatic nerve by adjacent masses or muscles can
result in symptoms such as sciatica and foot drop. The sciatic nerve is formed
from the L4-S3 sacral plexus nerve roots and exits the pelvis at the greater
sciatic notch. The 2 trunks of the sciatic nerve include the tibial nerve and the
common peroneal nerve, which are encased in a common epineural sheath.
Typically, the tibial and common peroneal nerves physically separate at the distal
thigh. In the pelvis, the sciatic nerve is closely associated with the piriformis
muscle and typically courses anterior and inferior to the piriformis muscle
(Figure 8.4). The sciatic nerve may also course through or above and posterior to
the piriformis muscle. Intrapelvic division of the sciatic nerve can also result in a
variety of anomalous courses; the common peroneal nerve may course through
or posterior to the piriformis muscle, and the tibial nerve may course anterior to
or through the piriformis muscle.4 Awareness of the sciatic nerve course is
critical when planning image-guided biopsies in the posterior hip and thigh.
Both the femoral and obturator nerves are formed from the L2-L4 lumbar
plexus nerve roots, within the psoas major muscle. The femoral nerve then
courses anteriorly along the surface of the iliopsoas muscle (Figure 8.5) and
subsequently beneath the inguinal ligament to exit the pelvis through the femoral
triangle. In contrast, the obturator nerve courses medial to the psoas muscle
(Figure 8.6) and exits the pelvis through the obturator canal.
FRACTURES
Proximal femur fractures may be subdivided as intracapsular and extracapsular
fractures. Intracapsular fractures include fractures of the femoral head and
femoral neck. Femoral neck fractures are further subdivided as subcapital
(femoral head-neck junction), transcervical (mid–femoral neck), and basicervical
(base of the femoral neck) fractures. Blood supply to the femoral head is
predominately from branches of the lateral circumflex and medial circumflex
arteries. Displaced intracapsular fractures may disrupt perfusion to the femoral
head and can result in avascular necrosis.5 Extracapsular fractures include
intertrochanteric and subtrochanteric fractures (Figure 8.7). Occult hip fractures
in women and older men following ground level falls may become a significant
source of morbidity (and even mortality) if undiagnosed. Radiographs should be
obtained first, and if negative or equivocal, MRI or CT should be obtained next,
depending on clinical circumstances and local availability.
•
FIGURE 8.1 Normal hip MRI. Selected axial PD images through the left hip at the
level of the A, supra-acetabular iliac bone, B, femoral head, and C, ischial tuberosity
show muscles of the hip. c, conjoint tendon of the biceps femoris and semitendinosus
tendon; gmax, gluteus maximus; gme, gluteus medius; gmi, gluteus minimus; i,
iliopsoas; oe, obturator externus; oi, obturator internus; p, pectineus; pi, piriformis; q,
quadratus femoris; r, rectus femoris; s, sartorius; sm, semimembranosus tendon; t,
tensor fascia lata.
•
FIGURE 8.2 Normal acetabular labrum. A, Axial T1 FS and B, coronal T1 FS MR
arthrogram of the left hip show the normal dark triangular appearance of the anterior
(white arrow), posterior (black arrow), and superior (arrowhead) labrum without intra-
articular contrast extending into the labrum or chondrolabral junction.
•
FIGURE 8.3 Normal sublabral recess. Radial T1 FS MR arthrogram of the right hip
shows sublabral interposition of a small amount of contrast at the posterior labrum
(arrow), without intrasubstance or full-thickness labral extension of contrast,
consistent with a sublabral recess.
•
FIGURE 8.4 Normal sciatic nerve. Axial PD MRI of the left hip shows a normal-
appearing sciatic nerve (arrow) with distinct individual nerve fascicles, directly anterior
to the piriformis muscle (asterisk).
Patients with stress and insufficiency fractures of the pelvis and hip may
present with nonspecific symptoms. Stress and insufficiency fractures of the
pelvis and hip may occur at a variety of locations, including the sacrum,
subchondral femoral head, femoral neck, pubic rami, and supra-acetabular iliac
bone (Figures 8.8–8.11). Femoral neck stress fractures may manifest along the
medial aspect of the femoral neck affecting the compressive trabeculae or along
the lateral aspect of the femoral neck affecting the tensile trabeculae. Owing to
the tensile distracting forces, lateral femoral neck stress fractures are predisposed
to complete fractures.6 The imaging evaluation typically begins with radiographs
and then MRI. Radionuclide bone scan and CT may also be appropriate,
depending on clinical circumstances.
•
FIGURE 8.5 Normal femoral nerve. Axial PD MRI of the left hip shows normal
appearance of the femoral nerve (arrow) along the anteromedial surface of the
iliopsoas muscle.
•
FIGURE 8.6 Normal obturator nerves. A, Axial PD MRI of the left hip at the level of
the sacroiliac joints shows the obturator nerves (arrows) coursing posteromedial to
the psoas muscle. B, At the level of the supra-acetabular iliac bones, the obturator
nerves (arrows) course anterior and medial to the obturator internus muscles.
OSTEONECROSIS OF THE FEMORAL HEAD

Osteonecrosis (also called avascular necrosis) of the femoral head refers to the
death of bone and bone marrow elements in the epiphysis extending to the
subchondral plate. Causes of osteonecrosis include trauma; use of
glucocorticoids and alcohol; hematologic abnormalities, such as sickle cell
anemia and myeloproliferative disorders; Gaucher disease; radiation; and
chronic pancreatitis.7 Often, no underlying cause of osteonecrosis can be
identified.8 MRI findings of avascular necrosis include a subchondral geographic
area of bone outlined by a serpentine hypointense band on T1-weighted images
(Figure 8.12). The double line sign may be present, which refers to an outer rim
of hypointense signal bordered by an inner rim of hyperintense signal on T2 or
PD FS images. The outer hypointense rim is thought to correspond to sclerotic
bone and the inner hyperintense rim is thought to represent hyperemic
vascularized granulation tissue.9 The underlying bone marrow may demonstrate
a variety of signals depending on the underlying tissue composition. Preserved
bone marrow fat in early avascular necrosis will demonstrate T1 hyperintense
and T2 intermediate signal. Presence of hemorrhage will demonstrate T1 and T2
hyperintense signal. Fluid or cystic change will manifest as T1 hypointense and
T2 hyperintense signal. Advanced osteonecrosis is characterized by hypointense
signal on both T1- and T2-weighted images because of underlying fibrosis and
sclerosis.10 Other important factors to evaluate on MRI include percentage of
femoral head involvement, presence of femoral head collapse, and development
of secondary degenerative changes.11 Differential considerations for
osteonecrosis include subchondral insufficiency fracture and transient bone
marrow edema. Subchondral insufficiency fracture typically demonstrates a
hypointense fracture line paralleling the subchondral plate.
•
FIGURE 8.7 Intertrochanteric hip fracture. A, Coronal STIR and B, coronal T1 MRI
of the pelvis show heterogeneous STIR hyperintense signal within the
intertrochanteric left hip (white arrows), with associated serpiginous T1 hypointense
fracture line (black arrows). There is hyperintense signal within the surrounding
muscles.
•
FIGURE 8.8 Stress fracture of the sacrum. A, Coronal STIR and B, coronal T1 MRI
of the sacrum show patchy STIR hyperintense signal within the sacral ala bilaterally
(white arrows), with associated serpiginous vertically oriented T1 hypointense fracture
lines (black arrows).
TRANSIENT BONE MARROW EDEMA SYNDROME

Transient bone marrow edema syndrome is a potential cause of hip pain and is
characterized by transient self-limiting and reversible demineralization on
radiographs12 and bone marrow edema within the femoral head and neck on
MRI. Classically, transient bone marrow edema syndrome is described in women
during the third trimester of pregnancy and middle-aged men. The underlying
cause is unclear. On MRI, patients present with T2 hyperintense and T1
hypointense signal within the femoral head and neck, occasionally involving the
acetabulum (Figure 8.13). Associated joint effusion may be present.13 Unlike
avascular necrosis, transient bone marrow edema syndrome should not be
bordered by a hypointense margin.
•
FIGURE 8.9 Femoral neck stress fracture. A, Coronal PD FS and B, coronal PD
MRI of the right hip show patchy bone marrow edema (circle) with associated
hypointense incomplete fracture line (arrows) along the medial compressive side of
the femoral neck.
•
FIGURE 8.10 Stress fractures of the pelvis and hips in a 66-year-old man with
multiple medical conditions and worsening bilateral hip pain. A, Coronal T1 MRI
shows abnormal low signal intensity the normal fatty marrow in the supra-acetabular
regions (arrows) and femoral necks bilaterally. B, Coronal T2 FS MRI shows bilateral
supra-acetabular and bilateral femoral neck stress fractures (arrows).
MUSCLE AND TENDON INJURIES

Muscle strains and tendon injuries about the hip are common causes of sports-
related pain; they are also common injuries in ground level falls. Partial tendon
tears demonstrate increased signal extending through a portion of the tendon on
fluid-sensitive sequences. Partial tendon tears may be subtler and manifest as
increased or decreased tendon caliber, with or without increased signal,
sometimes indistinguishable from tendon degeneration. Complete tendon tears
manifest as full-thickness defects, with varying degrees of tendon retraction.
Occasionally, because of marked tendon retraction, the full extent of
musculotendinous abnormality may not be completely imaged within the field of
view, and MRI of the femur or abdomen may be necessary to fully evaluate the
injury. Muscle injuries can present as muscle strain, which is the indirect injury
and tear of the muscle fibers. Findings of muscle strain range from minimal
feathery increased signal on fluid-sensitive sequences to gross disruption and
retraction of torn muscle fibers with hematoma formation.14,15
Athletes involved in running and jumping can often injure their hamstring
muscles that are composed of the biceps femoris, semitendinosus, and
semimembranosus muscles. The biceps femoris and the semitendinosus tendons
form a conjoint tendon that attaches to the ischial tuberosity posteriorly. The
semimembranosus tendon attaches directly to the ischial tuberosity anteriorly
(Figure 8.14). Possible manifestations of injury to the hamstrings include
tendinosis, partial tendon tear, tendon avulsion from the ischial tuberosity, and
muscle strain (Figure 8.15).16
•
FIGURE 8.11 Stress fracture. Axial T2 FS MRI of the left hip in a marathon runner
shows a stress fracture within the left inferior pubic ramus (arrows).
•
FIGURE 8.12 Avascular necrosis. Coronal PD MRI of the left hip shows a
geographic area of bone marrow outlined by a serpentine hypointense border
(arrows), consistent with avascular necrosis.
•
FIGURE 8.13 Transient bone marrow edema in a 40-year-old woman with sudden
onset of left hip pain without trauma. A, Coronal T2 FS and B, axial T2 FS MR
arthrogram of the left hip show patchy bone marrow edema (arrows) without fracture
line identified. Conservative treatment was successful.
Greater trochanteric pain syndrome is a common cause of lateral hip pain and
is often due to abnormality of the tendons and bursa at the greater trochanter.17
Four facets form the bony surface of the greater trochanter: the superoposterior,
posterior, lateral, and anterior facets. The gluteus medius attaches to the
superoposterior and lateral facets, and the gluteus minimus attaches to the
anterior facet. The greater trochanteric bursa overlies the posterior facet.18
Additional bursae that may form include the subgluteus minimus bursa and
subgluteus medius bursa. Possible manifestations of greater trochanteric pain
syndrome on MRI include gluteus medius and minimus tendinosis and tendon
tear, with possible bursal fluid distention (Figures 8.16 and 8.17).19 Similar to
the rotator cuff of the shoulder, calcific tendinitis may also occur, for which
correlation with radiographs would be helpful.
•
FIGURE 8.14 Normal hamstring origin. A, Axial PD MRI of the left hip just distal to
the ischial tuberosity shows the semimembranosus (arrowhead) anterolaterally, the
biceps femoris (white arrow) posterolaterally, and the semitendinosus (black arrow)
posteromedially. B, Subsequent image at the ischial tuberosity shows the union of the
biceps femoris and the semitendinosus to form the conjoint tendon (black arrow)
posteriorly and the semimembranosus (arrowhead) anteriorly.
•
FIGURE 8.15 Avulsion of the hamstring tendons from the ischial tuberosity. Axial T2
FS MRI of the pelvis shows marked edema (arrowheads) surrounding the ischial
tuberosity, extending into the adductor musculature anteriorly and obturator internus
medially. The semimembranosus tendon stump is retracted minimally from the ischial
tuberosity (black arrow). The conjoint tendon is retracted more distally (not shown).
The sciatic nerve (white arrow) is surrounded by soft-tissue edema. fm, femur; is,
ischium.
The rectus femoris muscle, the most superficial muscle of the quadriceps
muscle group, is frequently injured, especially with sports requiring kicking.
There are 2 components of the rectus femoris origin: the direct head that attaches
to the anterior inferior iliac spine and the indirect head that attaches to the
superior acetabular ridge and the hip joint capsule. Slightly caudal from the
rectus femoris origin, the direct and indirect heads join to form the conjoined
tendon (Figure 8.18). Possible manifestations of rectus femoris origin injuries
include avulsion fracture, complete tear, partial tear, and muscle strain (Figures
8.19 and 8.20).20
ATHLETIC PUBALGIA
High-level athletes can often present with groin pain from a variety of causes,
ranging from inguinal hernias to muscle injury. Athletic pubalgia was initially
defined as inguinal pain, without hernia, demonstrated on clinical examination,
usually in athletes.21 Now, athletic pubalgia typically refers to musculotendinous
injury in the region of the pubis symphysis.22 Athletic pubalgia is often seen in
high-level athletes participating in sports that require twisting and torqueing at
the waist, kicking, and rapid side-to-side motions. MRI is the most optimal
imaging study for the evaluation of athletic pubalgia.
Anatomically, the pubis symphysis is composed of the pubic bones and the
interpubic articular disk between the bodies of the pubic bones. Multiple muscles
attach to the pubic symphysis, including the rectus abdominis, transversus
abdominis, external oblique, internal oblique, adductor longus, adductor brevis,
adductor magnus, pectineus, and gracilis muscles. The rectus abdominis and
adductor longus are the most important stabilizers and form a common
aponeurosis at the attachment to the pubic tubercle. MRI findings of athletic
pubalgia include tear of the rectus abdominis-adductor longus aponeurosis and
fluid between the aponeurosis and the pubic tubercle (Figure 8.21). Associated
findings include bone marrow edema within the pubis and muscle or tendon
abnormalities of the anterolateral abdominal and thigh adductor muscles.22
Stress fractures of the pubis represent another cause of athletic pubalgia (Figure
8.22).
•
FIGURE 8.16 Patient with greater trochanteric pain syndrome. A and B, Axial T2 FS
MR arthrogram of the left hip shows thickening of the gluteus medius tendon (arrow)
with interstitial hyperintense signal just distal to the greater trochanter, consistent with
partial tear. Surrounding edema (black arrowheads) in the gluteus medius muscle
represents muscle strain. Focal fluid adjacent to the greater trochanter (asterisk) is in
keeping with the greater trochanteric bursitis.
ACETABULAR LABRAL INJURIES

Patients with acetabular labral abnormalities may present with intractable
mechanical hip pain or snapping hip syndrome. Abnormalities of the labrum can
be identified noninvasively with MRI or MR arthrography. As with the glenoid
labrum, there is considerable variability in the appearance of the acetabular
labrum, but tears can be identified by high signal or discontinuities in the labrum
that are filled with fluid. Disruptions of the peripheral attachment of the labrum
to the bony acetabulum may also occur. The presence of a paralabral cyst is
highly associated with labral tear (Figure 8.23). Tears of the acetabular labrum
occur most frequently (90%) in the anterior-superior portion (Figure 8.24).3
FEMOROACETABULAR IMPINGEMENT
MRI is the preferred imaging study for the evaluation of femoroacetabular
impingement (FAI), a condition that has been recently recognized and is still
controversial. In FAI, there is a mismatch in the size and geometry of the
femoral head and acetabulum, such that there is symptomatic impingement at the
extremes of motion. Cam-type impingement manifests as aspherical morphology
of the femoral head with prominent osseous protrusion at the anterolateral
femoral head-neck junction. With hip flexion, the femoral head can impact the
anterosuperior acetabular rim, resulting in damage to the anterosuperior labrum,
cartilage, and subchondral bone (Figure 8.25). There are various methods for
measuring the geometry of the femoral head. Pincer-type impingement results
from overcoverage of the proximal femur by the acetabular rim. Common causes
of pincer-type FAI include acetabular retroversion and acetabular protrusion.
Abnormalities of the posteroinferior cartilage and posterior and posteroinferior
labrum may be present on MRI.23
POSTARTHROPLASTY HIP
After hip arthroplasty, patients may present with hip pain. Radiographs are the
first-line imaging study and can evaluate for periprosthetic fracture and
loosening, osteolysis, and heterotopic bone formation. If there is clinical concern
for infection, hip aspiration is indicated. Radionuclide bone scans may also be
helpful in the evaluation of infection.24 If the cause of hip pain remains unclear,
MRI may be useful. However, hip MRI after arthroplasty can be challenging to
perform and interpret because of image degradation from susceptibility artifacts.
Techniques that help mitigate artifacts include imaging on lower magnetic field
strength, avoiding gradient-echo sequences, using STIR for fat saturation, using
a higher readout bandwidth, and imaging with thin sections. MRI scanners may
also have built-in proprietary and nonproprietary sequences for metal artifact
reduction.25
MRI can be useful in the evaluation of adverse local tissue reaction (ALTR),
radiographically occult stress reaction and fracture, synovitis, nerve injury,
iliopsoas impingement and tendinopathy, and gluteus medius and minimus
tendinopathy.26 ALTR describes the body’s reaction to metal debris and
corrosion products from arthroplasty wear and was classically described with
metal-on-metal arthroplasties. However, ALTR with metal-on-polyethylene
arthroplasties can also occur, especially with the advent of modular
arthroplasties that allow for metal corrosion at modular interfaces, a
phenomenon termed trunnionosis if the corrosion occurs at the head-neck
interface.27 ALTR can manifest on MRI as a pseudotumor that presents as a
mass in continuity with the hip arthroplasty. Pseudotumors may be
predominately fluid in signal with a thin wall or predominately solid (Figure
8.26). Dehiscence of the hip pseudocapsule can lead to decompression of fluid
and debris into the greater trochanteric bursa posterolaterally or iliopsoas bursa
anteriorly.26 Histopathologically, ALTR may present as an aseptic lymphocyte-
dominated vasculitis-associated lesion, which is a delayed type IV
hypersensitivity reaction to metal ions complexed with native proteins.28
•
FIGURE 8.17 Gluteus medius strain in a 75-year-old woman who had been walking
several miles per day. A, Axial T2 FS MRI at the level of the ilium shows feathery
edema in the gluteus medius muscle belly (arrow). There is no mass effect. B, Axial
T2 FS MRI at the level of the acetabular roof shows partial tear of the gluteus medius
tendon (arrow). C, Coronal T2 FS MRI shows extensive edema in the right gluteus
medius muscle belly and tear of the tendon. Fluid surrounds the detached tendon
(arrow).
MISCELLANEOUS CONDITIONS
Ischiofemoral impingement is a clinical syndrome of extra-articular hip pain that
is related to narrowing of the space between the ischial tuberosity and the
proximal femur.29,30 The quadratus femoris muscle can become impinged, as it
courses between the ischial tuberosity and proximal femur. MRI findings that
support the clinical diagnosis of ischiofemoral impingement include narrowing
of the ischiofemoral and quadratus femoris spaces, edema, atrophy, and fatty
infiltration of the quadratus femoris muscle (Figure 8.27). The ischiofemoral
space is demarcated by the lateral cortical margin of the ischial tuberosity and
the medial cortical margin of the lesser trochanter. The quadratus femoris space
is demarcated by the superolateral margin of the hamstring tendons and the
posteromedial aspect of the iliopsoas tendon or lesser trochanter.29 In a study, the
average ischiofemoral and quadratus femoris spaces measured approximately 23
and 12 mm, respectively, in control subjects without clinical evidence of
ischiofemoral impingement.29
•
FIGURE 8.18 Normal rectus femoris. A, Axial PD MRI of the left hip shows the
direct head of the rectus femoris (white arrow) attaching to the anterior inferior iliac
spine and the indirect head of the rectus femoris (black arrow) attaching to the
superior acetabular ridge. B, Caudally, the direct and indirect heads of the rectus
femoris join to form the conjoined tendon (arrowhead).
Piriformis syndrome is a controversial entity and has been described as a

potential cause of sciatica. At the greater sciatic notch, the sciatic nerve can
become compressed or irritated by the piriformis muscle. Potential causes of
piriformis syndrome include piriformis muscle spasm, hypertrophy, edema,
hematoma, and mass, or aberrant intramuscular course of the sciatic nerve.
Potential MRI findings that may support the clinical suspicion for piriformis
syndrome include asymmetric size of the piriformis muscle, abnormal signal of
the sciatic nerve, and loss of normal fat in the greater sciatic foramen.31,32
The iliopsoas bursa, the largest bursa in the human body, may communicate
with the hip joint through a deficiency within the joint capsule between the
iliofemoral and pubofemoral ligaments. Irritation or inflammation of the
iliopsoas bursa can lead to iliopsoas bursitis, a possible cause of hip pain.
Potential etiologies of iliopsoas bursitis include trauma, overuse injury, and
inflammatory arthritis. Exercises, such as running, that require repetitive hip
flexion and extension can result in mechanical irritation to the iliopsoas bursa.
MRI findings of iliopsoas bursitis include distended iliopsoas bursa with fluid
(Figure 8.28).33,34
•
FIGURE 8.19 Rectus femoris strain. A, Axial, B, coronal, and C, sagittal PD FS MRI
of the pelvis show edema surrounding the right rectus femoris with partial tear of the
indirect head of the rectus femoris (arrows).
•
FIGURE 8.20 Rectus femoris strain. A 20-year-old football player with quadriceps
strain. A-C, Coronal, sagittal, and axial PD FS MRI show the detached reflected head
of the rectus femoris surrounded by fluid (arrows).
•
FIGURE 8.21 Athletic pubalgia. A, Sagittal and B, axial oblique PD FS MRI show a
thin linear tear (arrows) of the left rectus abdominis-adductor longus aponeurosis at
the pubic attachment.
•
FIGURE 8.22 Stress fracture of pubic symphysis in a 21-year-old runner. A and B,
Axial T2 FS and coronal STIR MRI show high signal in the left pubis (arrows).
•
FIGURE 8.23 Labral tear. A, Radial and B, sagittal T1 FS MR arthrogram of the left
hip show a large tear of the anterosuperior labrum (white arrows) extending to the
superior labrum. C, Axial T2 FS MRI shows the associated paralabral cyst (black
arrow) adjacent to the superior labrum.
•
FIGURE 8.24 Labral tear in a 29-year-old woman with hip pain. Radial PD FS MR
arthrogram of the hip shows labral tear (arrow) at the anterosuperior labrum.
FIGURE 8.25 • A 31-year-old man with right hip pain and CAM-type
femoroacetabular impingement. A, Axial T1 FS MR arthrogram of the right hip shows
focal osseous bump (black arrow) at the femoral head-neck junction. B, Sagittal T1
FS MRI shows a small tear of the anterior-superior labrum (white arrow).
•
FIGURE 8.26 Pseudotumor formation after hip arthroplasty. A, Axial T2 MRI of the
left hip shows fluid collection (asterisk) surrounding the hip arthroplasty, extending
through a defect of the pseudocapsule posteriorly and into the greater trochanteric
bursa. B, Subtraction axial T1 FS Gd MRI shows enhancing nodular thickening
(arrow) adjacent to the greater trochanter.
•
FIGURE 8.27 Ischiofemoral impingement. Axial T2 FS MRI of the right hip shows
narrowing of the ischiofemoral space with marked atrophy and edema within the
quadratus femoris muscle (arrow).
•
FIGURE 8.28 Iliopsoas bursitis. Axial T2 FS MRI of the right hip shows fluid
distending the iliopsoas bursa (arrow) with associated reactive bone marrow edema in
the acetabulum (arrowheads).
References
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sublabral recess as a normal variant and a labral tear. Radiology. 2008;249:947–954.
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7. Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg
Am. 1995;77:459–474.
8. Lavernia CJ, Sierra RJ, Grieco FR. Osteonecrosis of the femoral head. J Am Acad Orthop Surg.
1999;7:250–261.
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radiographic staging, radionuclide imaging, and clinical findings. Radiology. 1987;162:709–715.
10. Saini A, Saifuddin A. MRI of osteonecrosis. Clin Radiol. 2004;59:1079–1093.
11. Steinberg ME, Hayken GD, Steinberg DR. A quantitative system for staging avascular necrosis. J Bone
Joint Surg Br. 1995;77:34–41.
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osteoporosis, transient bone marrow edema syndrome, or osteonecrosis. RadioGraphics. 1993;13:1001–
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associated factors. Arch Phys Med Rehabil. 2007;88:988–992.
18. Pfirrmann CW, Chung CB, Theumann NH, et al. Greater trochanter of the hip: attachment of the
abductor mechanism and a complex of three bursae—MR imaging and MR bursography in cadavers and
MR imaging in asymptomatic volunteers. Radiology. 2001;221:469–477.
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muscles as a cause of hip pain: MR imaging findings. AJR Am J Roentgenol. 1999;173:1123–1126.
20. Ouellette H, Thomas BJ, Nelson E, et al. MR imaging of rectus femoris origin injuries. Skeletal Radiol.
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technique and findings. RadioGraphics. 2008;28:1415–1438.
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characteristic MR arthrographic findings in 50 patients. Radiology. 2006;240:778–785.
24. Weissman BN, Palestro CJ, Appel M, et al. ACR Appropriateness Criteria® Imaging after Total Hip
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2004;183:63–64.
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1998;25:271–283.
1. Tears of the acetabular labrum are most frequently found on MRI at which
approximate clockface location?
A. 3 o’clock
B. 6 o’clock
C. 9 o’clock
D. 12 o’clock
2. Which of the following is an MRI feature of acute femoral neck stress

fracture?
A. High T1 signal
B. Bone marrow edema
C. Cortical thinning
D. Intense Gd enhancement
3. Tears of the acetabular labrum are most closely associated with which
condition?
A. Athletic pubalgia
B. Femoral head osteonecrosis
C. Sacral wing stress fracture
D. Femoroacetabular impingement
4. Athletic pubalgia is most closely associated with which muscles?

A. Gluteus medius and gluteus minimus
B. Semimembranosus and semitendinosis
C. Rectus abdominis and adductor longus
D. Rectus femoris and vastus lateralis

1. A Acetabular labral tears are usually anterior.
2. B Acute stress fractures typically show bone marrow edema.
3. D Acetabular labral tears are most closely associated with femoroacetabular
impingement.
4. C Athletic pubalgia may be caused by injuries of the aponeurosis of the
rectus abdominis and adductor longus.
9
MRI of Wrist and Hand Injuries
This chapter covers MRI techniques, anatomy, and MRI findings of injuries of
the wrist and hand.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of MRI of wrist and hand injuries, the learner will be
able to
4. summarize relevant concepts and knowledge for the following topics: anatomic variants and
pitfalls, bone injury, ulnar impaction syndrome, ligament and triangular fibrocartilage complex
(TFCC) injury, myotendinous injury, and nerve entrapment.
IMAGING TECHNIQUE
Recent technical advances in pulse sequence and extremity coil design allow
high-resolution examination of the complex anatomy of the wrist and hand.1,2
Imaging of this region may be performed at 1.5 T, but imaging at 3 T provides an
increased signal to noise ratio that allows significant improvement in spatial
resolution without increasing image time. The wrist should be in neutral position
during imaging and should be scanned from the distal radius to the proximal
metacarpals. Imaging of the thumb and fingers needs special attention on how to
acquire images. The axial images of the wrist should be parallel to the articular
surface of the distal radius, and for the thumb, axial images should be
perpendicular to the midshaft of the proximal phalanx. In our institution, sagittal
proton density (PD), axial T2 fat-saturated (FS), coronal T1, coronal T2 FS, and
axial and coronal gradient echo (GRE) sequences are obtained for routine wrist
MRI. For MR arthrography of the wrist, axial T2 FS, coronal T1, coronal T2 FS,
coronal GRE, and sagittal T2 FS sequences are obtained. The parameters used
include field of view of 10 to 12 cm, slice thickness of 3 mm, slice gap of
0.3 mm, and 172 to 332 × 145 to 230 matrix. For MR arthrography of the thumb,
axial T1 FS, T2 FS, sagittal T1, coronal T1 FS, and STIR sequences are
performed with the following parameters: field of view of 8 cm, slice thickness
of 2.5 to 3 mm, slice gap of 0 mm, and 224 to 260 × 112 to 144 matrix.
DICTATION CHECKLIST
Our dictation checklist for wrist MRI includes bones and bone marrow, joint
alignment and ulnar variance, articular cartilage, scapholunate and lunotriquetral
intrinsic ligaments, extrinsic wrist ligaments, triangular fibrocartilage complex
(TFCC), flexor and extensor tendons and tendon sheaths, muscles, joint fluid and
synovium, median and ulnar nerves, focal lesions, cysts and masses, and
subcutaneous tissues. Each of these sets of structures should be identified and
evaluated for morphology and signal characteristics. Any region of high T2
signal should attract further scrutiny. The clinical indication should be
specifically addressed.
OSSEOUS ANATOMY
Bones of the wrist form 3 articulations composed of the distal radioulnar joint
(DRUJ), radiocarpal joint, and midcarpal joints.1–3 The distal radius has the
radial styloid along its radial side and has articular fossae for the scaphoid and
lunate. The distal radial articular surface normally angles 24° toward the ulna in
the coronal plane and 12° to 15° toward the volar in the sagittal plane. There is a
notch in the ulnar side of the radius termed the sigmoid notch that articulates
with the distal ulna. The head of the ulna articulates with the lunate and
triquetrum distally separated by the TFCC. The styloid process projects from the
posteromedial aspect of the distal ulna and is separated from the ulnar head by a
narrow groove for the extensor carpi ulnaris (ECU). The 8 carpal bones are
organized into proximal and distal rows. The proximal carpal row consists of the
scaphoid, lunate, triquetrum, and pisiform bones, and the distal row consists of
the trapezium, trapezoid, capitate, and hamate bones. The articular surfaces of
the carpal bones are normally aligned into 3 arcs (Figure 9.1).4 Arc I represents
the proximal articular surfaces of the proximal row (except pisiform). Arcs II
and III represent the parallel articular surfaces at the midcarpal joint, with arc II
connecting the distal margins of the proximal row (except pisiform) and arc III
connecting the proximal margins of the capitate and hamate. A break in the
continuity of these arcs indicates the presence of a fracture or dislocation. The
osseous structures of the hand consist of the metacarpals and proximal, middle,
and distal phalanges. Along the carpometacarpal joints, the second through fifth
metacarpals form roughly the letter M. The articulations of the hand include the
metacarpophalangeal (MCP), proximal interphalangeal (PIP), and distal
interphalangeal (DIP) joints. The thumb lacks a middle phalanx. The MCP and
interphalangeal joints are structurally similar. They are both condyloid in
morphology, with a rounded head proximally articulating with a concave distal
articular surface (hinge-type joints). The shape of the articular surface allows a
greater degree of flexion than extension.
•
FIGURE 9.1 Carpal osseous anatomy. Posteroanterior radiograph of the wrist. It
shows the osseous structures. C, capitate; H, hamate; L, lunate; P, pisiform; R, radius;
S, scaphoid; Tq, triquetrum; TZ, trapezium; Tz, trapezoid; U, ulna. The radial sigmoid
notch (arrow) articulates with the ulnar head. Arc I, yellow line; Arc II, red line; Arc III,
blue line.
LIGAMENTS AND TENDONS
The TFCC is a main stabilizer of the DRUJ. In addition, it cushions the ulnar
head during axial loading and anchors it to the distal radius (Figure 9.2A). It is
composed of 5 structures: the triangular fibrocartilage (TFC) proper with volar
and dorsal radioulnar ligaments, the meniscus homologue, the ulnar collateral
ligament (UCL), the volar ulnocarpal ligaments (ulnotriquetral ligament and
ulnolunate ligament), and the sheath of the ECU tendon. The TFC is a dome-
shaped fibrocartilaginous structure and is best seen on coronal images. The ulnar
aspect is 2 to 3 times thicker. The center of the disk is biconcave and may be
quite thin or even fenestrated. The volar and dorsal margins of the disk are
thickened, called the radioulnar ligaments (Figure 9.2B). The meniscus
homologue is a triangular-shaped connective tissue found between the styloid
process, UCL, and triquetrum. The UCL extends from the styloid process to the
medial margin of the triquetrum. The volar ulnolunate and ulnotriquetral
ligaments arise from the volar aspect of the middle third of the disk and insert on
the lunate and triquetrum (Figure 9.2C). The ECU tendon sits in a groove along
the medial aspect of the ulna and inserts at the base of the fifth metacarpal.
The intrinsic carpal ligaments originate and insert onto the carpal bones and
act to restrict motion between the carpal bones.5 The 2 most important intrinsic
ligaments are the scapholunate and lunotriquetral ligaments. These ligaments are
C-shaped and are thicker dorsally and ventrally, with a thin central membranous
portion. The dorsal portion of the scapholunate ligament is thicker than the volar
portion and is most important for stability (Figure 9.3). In contrast, the volar
component of the lunotriquetral ligament is thicker and stronger than the dorsal
component. The extrinsic carpal ligaments originate in the forearm, insert onto
the carpal bones, and are classified by their locations as either volar or dorsal.
The volar extrinsic ligaments are stronger than the dorsal ligaments. There are 3
radiocarpal ligaments, the radioscaphocapitate, short radiolunate, and long
radiolunate, and 2 ulnocarpal ligaments, ulnotriquetral and ulnolunate. Two
important dorsal extrinsic ligaments are the dorsal radiotriquetral and dorsal
intercarpal ligaments (Figure 9.5). These ligaments are best seen on coronal,
thin-section gradient images. The ligamentous anatomy of the MCP and
interphalangeal joints is similar; the collateral and volar ligaments incorporated
into the joint capsule. The collateral ligaments are strong cords that attach
proximally to depressions on the condylar heads and insert distally to the palmar
aspect of the base of the phalanges (Figure 9.4). The volar ligament (also called
the volar plate) is a fibrocartilaginous tissue attaching to the proximal edge of
the phalanges and spreading at the sides to merge with the collateral ligaments
(Figure 9.6). The collateral ligaments are seen on axial and coronal MRI. The
volar plate is best seen on sagittal images.
The tendons of the wrist are grouped into flexor and extensor compartments.
The extensor tendons are divided into 6 compartments on the dorsal aspect of the
wrist and are sequentially numbered from the radial to the ulnar side (Figure
9.7). These tendons lie superficial to the carpal bones and interosseous
ligaments. The flexor tendons are located on the volar aspect of the wrist and
reside either within or adjacent to the carpal tunnel. In each finger, the flexor
tendons are kept against the bone of the phalanges by a fibrous envelope that is
composed of discrete thickenings of the flexor tendon sheath that form the
annular pulleys and cruciform pulleys. The extensor tendons of the hand arise
from a common compartment in the dorsum of the wrist. Over the dorsum of the
PIP joint, the extensor tendon divides into 3 slips. The central slip is broad and
inserts on the middle phalanx. The 2 lateral slips merge with the tendons of the
lumbrical and the interosseous muscles and then insert on the distal phalanx. The
extensor tendons are held in place by an extensor hood apparatus at MCP joints.
Each hood apparatus is composed of both sagittal bands and transverse fibers.
The sagittal bands arise from the volar plate and fuse with the deep transverse
metacarpal ligament. The transverse fibers are contributed by the dorsal
interossei and lumbricals.
CARPAL TUNNEL AND GUYON’S CANAL

The carpal tunnel is a cone-shaped space along the volar surface of the hand
(Figure 9.8). It is bordered dorsally by the carpal bones and volarly by the flexor
retinaculum, also known as the transverse carpal ligament. The proximal margin
of the tunnel extends from the pisiform on the ulnar side to the scaphoid tubercle
on the radial side. Its distal margin extends from the hook of hamate on the ulnar
side to the trapezium on the radial side. The carpal tunnel contains 8 flexor
tendons (superficialis and profunda), the flexor pollicis longus tendon, and the
median nerve. Axial MRI is the most optimal imaging plane for evaluating the
contents of the carpal tunnel.
•
FIGURE 9.2 Triangular fibrocartilage (TFC) complex (different patients). A, Coronal
gradient echo (GRE) MRI. B, Axial GRE MRI. C, Coronal GRE MRI. Magnetic
resonance images show the insertions of the TFC on the prominence of the sigmoid
notch (arrow in A), the styloid process (long arrow in A), and the ulnar fovea
(arrowhead in A). The prestyloid recess is a fluid-filled space between the meniscus
homologue and the styloid process, which is an extension of the radiocarpal joint (* in
A). The dorsal (arrow in B) and volar (long arrow in B) radioulnar ligaments that
extend from the medial cortex of the distal radius to that of the styloid process are
shown. The volar ulnolunate (arrowhead in C) and ulnotriquetral (arrow in C)
ligaments are shown. E, extensor carpi ulnaris; MH, meniscus homologue.
•
FIGURE 9.3 Scapholunate (SL) and lunotriquetral (LT) ligaments. A, Coronal T2 FS
MRI. B, Axial T2 FS MRI. Images show the normal SL (arrowhead in A) and LT (arrow
in A) ligaments. The SL ligament is thicker dorsally (arrow in B). L, lunate; S,
scaphoid; T, triquetrum.
•
FIGURE 9.4 Collateral ligaments at the metacarpophalangeal (MCP) joint. Coronal
proton density FS MRI shows radial and ulnar collateral ligaments at MCP joints,
blending with and reinforcing the capsule. The collateral ligaments appear as sharply
defined low signal intensity bands arising in depressions on the radial and ulnar sides
of the metacarpal head (arrow) and extending distally toward the base of the proximal
phalanx (arrowhead).
•
FIGURE 9.5 Extrinsic ligaments in the wrist. A, B. Coronal gradient echo MRI.
Images show the volar radioscaphocapitate (arrows in A), long radiolunate
(arrowhead in A), dorsal radiotriquetral (arrows in B), and dorsal intercarpal
(arrowheads in B) ligaments. L, lunate; R, radius; S, scaphoid.
•
FIGURE 9.6 Volar plate. Sagittal proton density FS MRI shows normal volar plate
(arrows).
On the ulnar side of the carpal tunnel, the flexor retinaculum divides and
creates a second tunnel known as Guyon’s canal. It is a fibro-osseous tunnel that
contains the ulnar nerve, the ulnar artery, and ulnar veins.
•
FIGURE 9.7 Normal extensor tendons of the wrist. Axial T2 FS MRI shows extensor
tendon compartments: 1, abductor pollicis longus, extensor pollicis brevis; 2, extensor
carpi radialis longus, extensor carpi radialis brevis; 3, extensor pollicis longus; 4,
extensor digitorum and indicis; 5, extensor digiti minimi; 6, extensor carpi ulnaris;
arrow, Lister’s tubercle.
•
FIGURE 9.8 Carpal tunnel and flexor tendons of the wrist. Axial T2 FS MRI shows
flexor tendons and the carpal tunnel. Arrow, flexor retinaculum; C, capitate; FCR,
flexor carpi radialis; FCU, flexor carpi ulnaris; FDP, flexor digitorum profundus; FDS,
flexor digitorum superficialis; FPL, flexor pollicis longus; H, hamate; MN, median
nerve; TZ, trapezium; Tz, trapezoid; UN, ulnar nerve.
•
FIGURE 9.9 Lunotriquetral coalition on coronal T1 MRI.
•
FIGURE 9.10 Type 2 lunate on coronal gradient echo MRI. The lunate (L) has 2
facets (arrows) for capitate (C) and hamate (H).
ANATOMIC VARIANTS AND PITFALLS

There are many anatomic variants and imaging pitfalls in MRI of the wrist and
hand.6,7
Lunotriquetral Coalition
Congenital fusions of the carpal bones may be fibrous, cartilaginous, or osseous.
Lunotriquetral coalitions are most common, followed by the capitohamate.
Lunotriquetral coalitions occur more commonly in the black population, have a
female predilection, and are frequently bilateral (about 60%). In conjunction
with lunotriquetral coalition, widening of the scapholunate joint is frequently
seen, which seems to be a normal variant. Lunotriquetral coalition is usually an
incidental finding (Figure 9.9).
Type 2 Lunate
Two distinct types of lunate can be identified normally. The lunate may have 1
distal facet articulating with the capitate (type 1) or 2 facets with additional
medial facet articulating with the hamate (type 2). The type 2 lunate is a little
more common (50%-65%) (Figure 9.10). The type 2 lunate has been frequently
associated with cartilage damage on the proximal pole of the hamate and may be
a cause of ulnar-sided wrist pain.
•
FIGURE 9.11 Os styloideum (arrow) on axial T2 FS MRI. There is a small ossicle
with marrow edema between the second and third metacarpophalangeal joints. C,
capitate.
Carpal Boss
The carpal boss is the clinical finding of a bony protuberance along the dorsum
of the wrist between the base of the second and third metacarpals. This may be
caused by degenerative or posttraumatic osteophytes or an accessory ossicle, the
os styloideum. The os styloideum may sometimes be fused with the base of the
metacarpal bone and is most easily recognized on cross-sectional images (Figure
9.11). Patients may present with wrist pain and limitation of motion caused by
associated osteoarthritis, overlying ganglion, or bursitis.
Ulnar Variance
Ulnar variance refers to the position of the distal articular surface of the ulna
relative to the adjacent distal articular surface of the radius in the longitudinal
dimension. If the surfaces are aligned, there is neutral ulnar variance (see Figure
9.1). If the ulna protrudes distally beyond the radius, there is positive ulnar
variance. If the ulna is shorter than the radius, there is negative ulnar variance.
There is no generally accepted normal range of ulnar variance measurements,
and the relative lengths of the ulna and radius vary with positioning and
radiographic technique. The standard position for measurement is a seated
patient with 90° shoulder abduction, 90° elbow flexion, and the wrist relaxed in
pronation; the X-ray beam is centered at the carpus with 90° incidence. This
position generally cannot be obtained during MRI, but conditions related to ulnar
variance often have MRI findings.
Triangular Fibrocartilage Complex

The TFC is a fibrocartilaginous disk that is hypointense on MRI. However, the
radial and ulnar attachments of the TFC often show an intermediate to high
signal that may be misinterpreted as a tear. The ulnar attachment of the TFC is
composed of 2 distinct laminae that are separated by fibrovascular tissue
(ligamentum subcruentum). This can show an intermediate signal and internal
striations. At the radial attachment, hyaline cartilage curves around the radius
and may result in curvilinear high signal on fluid-sensitive sequences that could
be misinterpreted as a tear. In aging patients small defects may be seen normally
within the central portion of the TFC, the substance of the scapholunate and
lunotriquetral ligaments. Many of these defects have no clinical significance.
•
FIGURE 9.12 Accessory abductor digiti minimi (arrow) on axial T1 MRI. It is seen
radial and volar to the pisiform (P) and inserts with the abductor digiti minimi at the
ulnar base of the fifth proximal phalanx, projecting superficial to Guyon’s canal (*).
Tendons
The normal tendons of the wrist have low signal intensity on MRI. High signal
within tendons may reflect degeneration or tear. However, focal signal
abnormalities in tendons also can be seen as normal variants. Centrally increased
signal within the ECU tendon at the level of the DRUJ is a frequent normal
finding and may be related to interdigitation of 2 tendinous slips. Similarly, the
normal abductor pollicis longus (ABPL) tendon may have a striated appearance
related to the fusion of multiple tendinous bundles and interposed fat that can be
misinterpreted as a longitudinal tear. Increased signal within the extensor pollicis
longus tendon, distal to Lister’s tubercle, is frequently seen as a result of the
magic angle phenomenon.
Muscles
Anatomic variants of the hand muscles include the accessory abductor digiti
minimi, the extensor digitorum brevis (extensor digitorum brevis manus), as well
as variants of the lumbrical, the palmaris longus, and the flexor digitorum
superficialis muscles. The accessory adductor digiti minimi is the most common
of the accessory muscles and may be bilateral in 50% of cases (Figure 9.12).
Nerves
A bifid median nerve is an anatomic variation that may be associated with carpal
tunnel syndrome. It occurs when the median nerve splits either before entering
or within the carpal tunnel. A small percentage of the population (2%-4%) has a
persistent median artery located within the carpal tunnel. Although typically
asymptomatic, an enlarged persistent median artery may lead to carpal tunnel
syndrome by compressing the median nerve (Figure 9.13).
•
FIGURE 9.13 Bifid median nerve (arrows) and persistent median artery (PMA) on
axial T2 FS MRI.
WRIST AND HAND INJURIES

Wrist and hand injuries are common occurrences in all sports and various
activities of daily living. These are divided into 2 major classifications: traumatic
and overuse. Traumatic injuries include fractures, dislocations, and acute
ligament and tendon tears often seen in contact/collision sports. Overuse injuries
from sports are quite common, and these include chronic ligament and tendon
tears as well as impaction and impingement syndromes. These are frequently
seen in racket sports, rowing, and gymnastics. MRI has an important role in both
identifying and ruling out wrist and hand injuries.8–10
OSSEOUS INJURY
Scaphoid fractures are the most common and most problematic carpal bone
fractures. Scaphoid fractures are classified by location, stability, and time of
injury. Most acute fractures in athletes involve the scaphoid waist and are
minimally displaced. In pediatric patients, scaphoid fractures typically occur
more distal than the scaphoid waist, and these injuries are avulsions with little
associated marrow edema. These fractures are frequently seen in contact sports
(football, rugby) and sports involving high velocities (skating, rollerblading). In
athletes with clinical suspicion of scaphoid fracture and negative radiographs,
MRI is helpful to diagnose occult fractures and to avoid unnecessary
immobilization (Figure 9.14). The goal of the treatment of acute scaphoid
fracture is to obtain union. The natural history of untreated scaphoid fractures
demonstrates nonunion and progressive radiocarpal arthritis, known as scaphoid
nonunion advanced collapse wrist.
The incidence of hook of the hamate fractures is 2% to 4% of all carpal
fractures. The injury usually occurs in athletes who participate in baseball, golf,
and racket sports because of the position of the implement in the hand (Figure
9.15A). Examination reveals tenderness over the hook of the hamate that lies on
a line between the pisiform and second metacarpal head. This is frequently
missed in clinical practice and routine radiographic views. Diagnosis is usually
confirmed with a CT scan (Figure 9.15B). Treatment of hook of the hamate
fractures in athletes varies from casting to open reduction and internal fixation to
excision.
•
FIGURE 9.14 Scaphoid waist fracture. Coronal T1 MRI shows scaphoid waist
fracture (arrow) associated with early avascular necrosis of the proximal pole with
partial collapse.
Stress fractures are uncommon in the upper extremity. Gymnast’s wrist

develops when there is repetitive trauma to the distal radial physis. It is seen in
as many as 80% of elite gymnasts. Patients become symptomatic around the age
of 12 to 14 years. Most patients are girls, and gymnast’s wrist is bilateral in one-
third of cases. Radiographs show a wide distal radial physis with irregular and
sclerotic borders. MRI shows increased T2 signal of the physis and paraphyseal.
With time, if gymnast’s wrist is untreated, this condition may result in premature
closure of the distal radial physis and subsequent symptoms related to positive
ulnar variance.
ULNAR IMPACTION SYNDROME
Ulnar impaction syndrome is caused by the impaction between the ulnar carpal
bones and the distal ulnar head.8,9,11 This can lead to ulnar-sided wrist pain and
degenerative condition of the DRUJ and ulnocarpal compartment. This
syndrome is commonly seen in gymnasts and players of racket sports.
Radiographs commonly show positive ulnar variance. Other findings include
sclerosis or cystic change at the ulnar aspect of the proximal lunate, triquetrum,
and ulnar head. MRI may demonstrate TFCC degenerative tear, chondromalacia,
bone marrow edema, subchondral cysts, or lunotriquetral ligament tear (Figure
9.16).
LIGAMENT INJURY
Scapholunate ligament injuries, the most common type of wrist ligament injury,
are common in collision and contact sports or any activity where a fall may
occur.8,9 Injury to the scapholunate ligament may be partial or complete. After
the ligament disruption, the scaphoid assumes a flexed position and the lunate
and triquetrum tilt dorsally, producing a dorsal intercalated segment instability.
Over time, progressive osteoarthritis will occur, known as scapholunate
advanced collapse wrist (Figure 9.17). Coronal and axial MRI are the best for
direct assessment of the scapholunate ligament. A partial tear appears as focal
thinning, irregularity, or increased signal intensity. It most commonly involves
the volar portion of the ligament, which is the weakest point. A complete tear is
characterized by a discontinuity or complete absence of the ligament. On MR
arthrography, a complete scapholunate ligament tear results in communication
between the radiocarpal and midcarpal joints (Figure 9.18). Ancillary signs
include associated tears of the volar extrinsic radiocarpal ligaments, scaphoid or
lunate chondromalacia, bone marrow edema, and secondary osteoarthritis.
•
FIGURE 9.15 Hook of hamate fracture. A, Diagram. B, Axial CT. The diagram
demonstrates the mechanism of injury that is thought to be caused by abutment of the
hook on an object or by a shearing force applied by the flexor tendon of the small and
ring fingers. The CT image shows the fracture of hook of hamate (arrow). C, capitate;
H, hamate; S, scaphoid; Tm, trapezium.
•
FIGURE 9.16 Ulnar impaction syndrome. Coronal T2 FS MRI shows triangular
fibrocartilage tear (short arrow), chondromalacia of lunate (long arrow), bone marrow
edema and subchondral cysts at ulnar head and lunate.
Lunotriquetral ligament injuries are much less common than scapholunate

ligament injuries. Although complete scapholunate ligament disruption
frequently leads to dorsal intercalated segment instability, lunotriquetral ligament
tears are rarely associated with a volar intercalated segment instability pattern
because of the presence of secondary stabilizers such as dorsal and volar
extrinsic ligaments. Therefore, lunotriquetral injuries, as opposed to
scapholunate injuries, usually do not lead to progressive arthritis. Complete or
partial lunotriquetral disruptions demonstrate MRI findings similar to
scapholunate tears. In acute lunotriquetral injuries, immobilization is the initial
treatment of choice.
DRUJ and TFCC injuries are common in athletes and may be the result of
acute traumatic injury or repetitive trauma. Acute traumatic events involve axial
loading with rotational stress, usually due to a fall on the outstretched hand.
Another mechanism of TFCC injury may occur from repetitive trauma; a
distraction force applied to the volar wrist, frequently seen in racket sports.
TFCC injury and ulnar wrist pain are common in gymnasts, racket players,
hockey players, golfers, and boxers.
Palmer12 devised a classification system for TFCC injuries that is based on
the cause, location, and extent of the injury. This classification system has been
well received and has significant implications for treatment planning (Table 9.1).
On MRI, TFC tears demonstrate linear fluid signal on T2 MRI. CT or MR
arthrography increases diagnostic accuracy of foveal tears when comparing with
conventional MRI and allows assessment of associated small bone avulsions. On
MR arthrography, a complete tear of the TFCC results in communication
between the radiocarpal joint and the DRUJ (Figure 9.19).
Collateral ligament injuries of the thumb MCP joint are quite common in all
sports.8–10 The primary mechanism of injury is an abrupt abduction stress to the
UCL. A skier with a ski pole sustaining a fall may result in radial stress on the
thumb at the time of injury. UCL injuries are common and much more frequent
than radial collateral ligament injuries. This skier’s or gamekeeper’s thumb is
frequently seen in football, basketball, and other contact collision sports. Most
UCL injuries occur at the attachment to the proximal phalanx. Partial UCL tears
can be treated by simple immobilization, whereas complete UCL injuries with
Stener lesions should be treated surgically. In a Stener lesion, the distal portion
of the UCL avulses from its attachment on the proximal phalanx and herniates
through the adductor aponeurosis. MRI demonstrates a yo-yo on a string
appearance with the string representing the adductor aponeurosis and the yo-yo
representing the balled-up and proximally retracted UCL (Figure 9.20).
•
FIGURE 9.17 Scapholunate advanced collapse wrist. Anteroposterior radiograph of
the wrist shows widening of scapholunate interval (double-headed arrow) owing to
scapholunate ligament injury. There is associated osteoarthritis at radiocarpal joint.
•
FIGURE 9.18 Intrinsic ligament injury of the wrist. Coronal gradient echo MR
arthrography shows disruption of scapholunate (arrow) and lunotriquetral (arrowhead)
ligaments. There is intra-articular contrast communication between the radiocarpal
and midcarpal joints.
Table 9.1 TRIANGULAR FIBROCARTILAGE COMPLEX ABNORMALITIES BY PALMER

CLASSIFICATION
Class 1: Traumatic
A. Central perforation
B. Ulnar avulsion
With distal ulnar fracture
Without distal ulnar fracture
C. Distal avulsion
D. Radial avulsion
With sigmoid notch fracture
Without sigmoid notch fracture
Class 2: Degenerative (ulnocarpal abutment syndrome)

A. Triangular fibrocartilage complex (TFCC) wear
B. TFCC wear and lunate and/or ulnar chondromalacia
C. TFCC perforation and lunate and/or ulnar chondromalacia
D. TFCC perforation and lunate and/or ulnar chondromalacia and
lunotriquetral ligament perforation
E. TFCC perforation and lunate and/or ulnar chondromalacia and
lunotriquetral ligament perforation and ulnocarpal arthritis
Based on Palmer AK. Triangular fibrocartilage complex lesions: a

classification. J Hand Surg Am. 1989;14:594–606.
•
FIGURE 9.19 Triangular fibrocartilage complex (TFCC) tear. Coronal T1 FS MR
arthrography shows TFCC tear from the ulnar attachment site (black arrow) results in
communication between the radiocarpal joint and the distal radioulnar joint (white
arrow).
Volar plate injuries at the PIP joint can be isolated or associated with
collateral ligaments tears. They occur from hyperextension of the PIP joint or
rotational longitudinal compression, which is common in ball-handling sports.
Radiographs may demonstrate avulsion fractures at the base of the middle
phalanx. MRI is more sensitive by directly visualizing the detached volar plate
or fluid signal within the volar plate on fluid-sensitive sequences (Figure 9.21).
•
FIGURE 9.20 Stener lesion. Coronal STIR MR arthrography demonstrates ulnar
collateral ligament tear at the distal aspect (arrow) with interposed adductor
aponeurosis resulting in “yo-yo on a string” appearance.
•
FIGURE 9.21 Volar plate injury. Sagittal T2 FS MR arthrography shows irregularity
and increased signal of the volar plate at the metacarpophalangeal joint (arrow).
The extensor hood mechanism includes sagittal bands that attach from the
extensor tendon to the volar plate and the transverse and oblique reticular fibers
from the intrinsic muscles of the hand. Injuries to the extensor hood can occur
from a direct blow and sudden forced flexion of the MCP joints. Boxer’s knuckle
refers to extensor tendon dislocation associated with repetitive injury of the
sagittal band. The term came about owing to a high incidence of this injury
among boxers, often incurred when landing a punch. The middle finger is the
most commonly injured because of its thin and long radial sagittal band and
prominent metacarpal head. On axial MRI, discontinuity and abnormal signal
intensity of the sagittal band can be seen associated with subluxation or
dislocation of the extensor tendon (Figure 9.22).
•
FIGURE 9.22 Sagittal band rupture. Axial T2 FS MR arthrography shows tear of the
radial sagittal band (white arrow). The ulnar sagittal band (black arrow) is intact. ET,
extensor tendon.
Focal thickenings of the flexor tendon sheath comprise a series of pulleys that
maintain the flexor tendon in close apposition to subjacent bone. The pulley
system is made up of 5 annular and 3 cruciate pulleys through which the flexor
tendons glide (Figure 9.23A). Pulley injuries can be seen in activities that
impose stresses on the supporting structures of the fingers, such as rock
climbing. In rock climbers, the injury usually occurs upon sudden force that
extends the fingers while already in a hanging position. The A2 pulley is
commonly involved. In baseball pitchers, an isolated A4 injury is typically
observed. On axial MRI, discontinuity, nonvisualization, and edema of the
pulleys can be seen (Figure 9.23B). Sagittal MRI is best to observe the
bowstring appearance of the flexor tendon. In A2 pulley tears, maximal
bowstring is seen over the proximal phalanx, whereas in A4 pulley tears
maximal bowstringing is seen over the middle phalanx.
TENDON INJURY
De Quervain syndrome is the most common wrist tendinopathy in athletes.8,9
This painful stenosing tenosynovitis results from repetitive gliding of the ABPL
and extensor pollicis brevis tendons over the radial styloid (Figure 9.24). Sports
requiring forceful grip coupled with ulnar deviation or repetitive use of the
thumb predispose the athlete to this disorder. These sports include golf, fly
fishing, and racket sports. MRI may demonstrate hypertrophy of the first dorsal
compartmental retinaculum, tenosynovial effusion with thickening, hypertrophy
and heterogeneous appearance of the tendons, and surrounding soft-tissue
edema.
Intersection syndrome is an inflammatory process of the second extensor
compartment tendons of the wrist (extensor carpi radialis longus and brevis), 4
to 8 cm proximal to Lister’s tubercle of the distal radius. Peritendinitis occurs
where the first extensor compartment tendons (ABPL and extensor pollicis
brevis) cross over the second extensor compartment tendons, mostly related to
chronic overuse. This syndrome is association with sports requiring repetitive
wrist extension such as rowing, racket sports, horseback riding, and skiing.
Fluid-sensitive MR sequences are the most useful for demonstrating changes of
peritendinitis including tendon thickening and tenosynovial fluid surrounding the
second and the first extensor compartments extending proximally from the point
of crossover.
•
FIGURE 9.23 Annular pulley tear. A, Diagram shows the normal fibro-osseous
tunnel composed of 5 pulleys (A1-A5) stabilizing the flexor tendons. B, Axial proton
density FS MRI shows tear of the A2 annular pulley at the level of the proximal
phalanx (arrow). There is bowstringing of the flexor tendon (double-headed arrow).
DP, distal phalanx; MCP, metacarpal; MP, middle phalanx; PP, proximal phalanx.
•
FIGURE 9.24 de Quervain syndrome. Axial T2 FS MRI shows tendinosis of
abductor pollicis longus and extensor pollicis brevis tendons with fluid in the tendon
sheath (arrow).
FIGURE 9.25 • Extensor carpi ulnaris (ECU) tear. Axial T2 FS MRI shows
longitudinal split tear of the ECU (arrow).
Tenosynovitis of the ECU in the sixth dorsal compartment is common, second

only to de Quervain syndrome.11 The ECU is held within the groove of the ulnar
head by a deep retinaculum, called the ECU subsheath. ECU tenosynovitis is
seen in sports requiring repetitive wrist motion, such as rowing and racket sports,
and is quite common in the nondominant wrist of tennis players caused by the 2-
handed backhand. On MRI, thickening of the tendon sheath, tenosynovial
effusion, and peritendinous inflammatory changes are demonstrated. Chronic
stenosing tenosynovitis demonstrates peritendinous low signal intensity and an
irregular margin from scarring. Partial tears can result from chronic attrition of
the tendon in patients with underlying instability or chronic stenosing
tenosynovitis (Figure 9.25).
Closed tendon injuries in fingers are frequent and include boutonniere injury,
mallet finger, and jersey finger.10 Boutonniere injury is a traumatic injury of the
central slip of the extensor tendon at its insertion into the base of the middle
phalanx (Figure 9.26). It results from forced flexion of a rigidly extended PIP
joint. It is commonly seen in basketball players and martial arts participants who
use open hand blocking techniques. Over time, with or without bony avulsion of
the middle phalangeal base, flexion at the PIP joint and extension at the DIP joint
occur, which give rise to a boutonniere deformity. Mallet finger is usually caused
by acute forceful flexion of the extended DIP joint from direct trauma. An injury
of the terminal extensor tendon occurs with or without bony avulsion from the
dorsal base of the distal phalanx (Figure 9.27). Mallet finger clinically manifests
as a flexion deformity of the DIP joint and is commonly seen in players of sports
such as baseball, basketball, and volleyball. Jersey finger is an avulsion of the
flexor digitorum profundus tendon from the volar insertion to the distal phalanx
(Figure 9.28). This injury results from a forced extension of the flexed DIP joint
as mostly occurs when a player grabs a moving player’s jersey. Radiographs are
an important initial imaging modality to visualize avulsion injuries of finger
tendons. MRI may be helpful for clinically equivocal cases to demonstrate
osseous injury, discontinuity, and level of retraction of the injured tendons.
•
FIGURE 9.26 Boutonniere injury (different patients). A, Lateral radiograph. B,
Sagittal STIR MRI. A dorsal avulsion fragment from the middle phalanx is seen (arrow
in A). MRI shows injury of the central slip of the extensor tendon at its insertion into
the base of the middle phalanx (arrow in B).
•
FIGURE 9.27 Mallet finger. Lateral radiograph shows the dorsal avulsion fragment
from the distal phalanx (arrow).
•
FIGURE 9.28 Jersey finger. Lateral radiograph shows hyperextension of distal
interphalangeal joint because of flexor digitorum profundus tendon injury (arrow).
•
FIGURE 9.29 Median neuropathy in a rock climber. Axial T2 FS MR arthrography
shows enlarged median nerve in a carpal tunnel (arrow).
NERVE ENTRAPMENT
Carpal tunnel syndrome may occur as a result of compression of the median
nerve in the carpal tunnel secondary to tenosynovitis of the flexor tendons in
athletes.13 MRI may show edema and enlargement of the median nerve and may
also display predisposing factors such as flexor tenosynovitis (Figure 9.29).
Guyon’s canal syndrome refers to the compression of the ulnar nerve in the
Guyon’s canal. Handlebar palsy refers to the isolated compressive neuropathy of
the motor branch of the ulnar nerve in cyclists related to prolonged riding with
the hands pressed against the handlebars. Furthermore, a displaced hook of the
hamate fracture is a well-known cause of ulnar neuropathy. MRI can show
swelling and edema of the nerve proximal to the canal, and its flattening within
the canal, best appreciated on axial MRI.
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606.
13. Miller TT, Reinus WR. Nerve entrapment syndromes of the elbow, forearm, and wrist. AJR Am J
1. Which finding on wrist MR arthrogram is normal (with radiocarpal

compartment injection)?
A. Contrast in the midcarpal compartment
B. Contrast in the distal radioulnar joint
C. Contrast in the carpometacarpal joints
D. Contrast in the piso-triquetral joint
2. MRI findings of peritendinitis on the dorsal side of the wrist are most closely
associated with which condition?
A. de Quervain syndrome
B. Intersection syndrome
C. Ulnar impaction syndrome
D. Carpal tunnel syndrome
3. The capitate typically articulates with how many other bones?

A. Four or fewer
B. Five
C. Six
D. Seven or more
4. Injury of which finger tendon is most closely associated with a posttraumatic

boutonniere deformity?
A. Terminal extensor tendon
B. Central slip of the extensor tendon
C. Flexor digitorum profundus tendon
D. Flexor digitorum superficialis

1. D The radiocarpal compartment normally communicates with the piso-
triquetral articulation.
2. B Intersection syndrome occurs where the wrist extensor tendons cross each
other, on the dorsal side of the wrist.
3. D The capitate typically articulates with 3 metacarpals, the hamate, the
scaphoid, the lunate, and the trapezoid.
4. B Tear of the central slip of the extensor tendon allows unopposed flexion at
the PIP.
10
MRI of Ankle and Foot Injuries
Radiography should be the first imaging examination in the setting of ankle and
foot trauma. We typically recommend CT first if radiography leaves unresolved
issues. MRI is reserved for evaluation of soft-tissue structures in the subacute or
chronic setting, or persistent pain with negative radiographs and negative CT.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of MRI of ankle and foot injuries, the learner will be
able to
4. summarize relevant concepts and knowledge for the following topics: tendon injury, ligament
injury, bone trauma, impingement syndromes, stress injury, Lisfranc injury, and turf toe.
MRI TECHNIQUES
Our standard MRI technique at Brigham and Women’s Hospital treats the ankle
and hindfoot as the same anatomic region. We obtain images in axial, coronal,
and sagittal planes in combination with T1 and fluid-sensitive pulse sequences.
Our current protocol is sagittal T1 and STIR, axial PD and T2 FS, and coronal
PD and T2 FS. We could probably get by with only 1 sequence in each plane,
but we would never be able to agree on which sequence that would be. The
volume from distal tibia through heel and midfoot is covered. We also add an
axial PD oblique sequence to better visualize the ligaments and the peroneal
tendons. The exact technical parameters will vary with the scanner. For the
midfoot and forefoot, we use sagittal, transverse (short axis), and longitudinal
(long axis) imaging planes. The sagittal plane follows the space between the
second and third metatarsal shafts, the longitudinal plane approximates the plane
of the metatarsals, and the transverse plane is orthogonal to the longitudinal
plane. For injuries to the first metatarsophalangeal (MTP) joint (turf toe injury),
we have a specific forefoot protocol centered on the first MTP joint using T1 or
PD with additional FS or STIR in all 3 planes using a small 10- to 14-cm field of
view and 3 mm slice thickness.
DICTATION CHECKLIST
Our dictation checklist for ankle and hindfoot MRI includes bones and bone
marrow, joint alignment, articular cartilage, syndesmotic ligaments, medial and
lateral collateral ligaments, plantar and calcaneonavicular ligaments, plantar
aponeurosis, sinus tarsi, flexor and extensor tendons and tendon sheaths,
Achilles tendon, muscles, joint and bursal fluid, vessels and nerves, focal
lesions, cysts and masses, and subcutaneous tissues. Each of these sets of
structures should be identified and evaluated for morphology and signal
ANATOMY
All of the important ankle and foot structures should be identifiable on MRI
(Figures 10.1 and 10.2). The ankle mortise is formed by the distal tibia and
fibula and their articulation with the talus. The distal tibiofibular joint is a
fibrous joint (referred to as the syndesmosis) where the distal fibular metaphysis
rests within the fibular notch of the tibia and is supported by anterior and
posterior tibiofibular ligaments. The most distal portion of the fibula extends
inferior to the tibia as the lateral malleolus. The posterior lip of the distal tibia is
referred to as the posterior malleolus and receives the posterior tibiofibular
ligament. The articular surface of the distal tibia, called the tibial plafond, is
continuous with the articular surfaces of the medial and lateral malleoli. The
deltoid ligament attaches the medial malleolus to the talus (deep portion) and
calcaneus (superficial). The lateral collateral ligament has 3 parts: the anterior
talofibular ligament (ATFL), the calcaneofibular ligament, and the posterior
talofibular ligament (PTFL). Two talocalcaneal joints exist: subtalar (posterior
subtalar facet) and talocalcaneonavicular (anterior and middle subtalar facets),
which are separated by 2 spaces, the sinus tarsi and the tarsal tunnel. The sinus
tarsi is the lateral space located between the talus and calcaneus and contains fat,
blood vessels, nerves, and ligaments that stabilize the subtalar joint. The tarsal
tunnel is a fibrosseous tunnel located inferolateral to the sustentaculum tali,
between the flexor digitorum and the flexor hallucis longus (FHL) tendons, that
contains the posterior tibial nerve and the posterior tibial vessels.
•
FIGURE 10.1 Normal ankle anatomy. A, Axial PD MRI at the level of the
syndesmosis shows the ankle tendons. Anterior tendons: ED, extensor digitorum
longus; EH, extensor hallucis; TA, tibialis anterior. Posterior tendons: A, Achilles; FDL,
flexor digitorum longus; FHL, flexor hallucis longus; PB, peroneal brevis; PL, peroneal
longus; TP, tibialis posterior. The plantaris is anteromedial to the Achilles (arrowhead).
Fib, fibula; K, Kager fat pad. B, Coronal PD MRI through the ankle mortise shows
some of the ankle tendons and ligaments. The deep (long arrow) and superficial
(small arrow) portions of the deltoid ligament are visible. The calcaneofibular ligament
(short arrow) and the posterior talofibular ligament (PTFL) (arrowhead) are visible.
AbdH, abductor hallucis; ADM, adductor digiti minimi muscle; FDB, flexor digitorum
muscle; LM, lateral malleolus; MM, medial malleolus; TT, tarsal tunnel. The central
(black arrow) and lateral (black arrowhead) cords of the plantar aponeurosis are seen.
C, Sagittal T1 MRI through the midankle shows the sinus tarsi (ST). ACP, anterior
calcaneal process; C, cuboid; N, navicular. The central cord of the plantar
aponeurosis is visible (arrowhead). There is a small Stieda process (small arrow) of
the talus. D, Oblique axial PD MRI through the ankle mortise. The deep deltoid
ligament (long white arrow), the PTFL (arrowhead), and the posterior subtalar joint
(small white arrows) are visible. The calcaneofibular ligament lies deep to the PB and
PL tendons.
•
FIGURE 10.2 Anterior and posterior talofibular ligaments (PTFL). Axial PD FS MRI
shows the anterior talofibular ligament (arrowhead) and the PTFL (small arrow). A,
Achilles tendon; N, navicular; TP, tibialis posterior tendon.
The Achilles tendon extends from midcalf to the posterior calcaneal

tuberosity; when present, the plantaris tendon follows along its anteromedial
aspect. The peroneus brevis and longus tendons course posterior and then
inferior to the lateral malleolus, and they turn anteriorly to their insertions. The
peroneus brevis inserts at the lateral surface of styloid process of fifth metatarsal
base; the peroneus longus inserts at the plantar posterolateral aspect of medial
cuneiform and lateral side of first metatarsal base. The peroneal tendons are held
in place behind the lateral malleolus by the superior peroneal retinaculum (SPR),
a fibrous band that extends from the posterolateral distal fibula to the lateral
calcaneus, and the Achilles tendon aponeurosis. The FHL courses posterior to
the tibia and talus, then turns anteriorly underneath the talus, and then inserts on
the distal phalanx of great toe. Fluid is normally seen within the FHL tendon
sheath but not in the other ankle tendon sheaths. The tibialis posterior and the
flexor digitorum longus course posterior and then inferior to the medial
malleolus. The tibialis posterior divides into multiple slips and inserts on the
tuberosity of the navicular and plantar surfaces of the metatarsals and
cuneiforms. The flexor digitorum longus divides into slips that insert on the
plantar surfaces of the bases of distal phalanges of the lesser toes. Anatomic
variants at the posterior ankle include the accessory soleus, peroneus tertius, and
peroneus quartus muscles, and variations on the level of the musculotendinous
junctions. There are 3 anterior ankle tendons: the tibialis anterior is medial, the
extensor digitorum longus is central, and the extensor hallucis longus is lateral.
Several developmental ossicles are found within the ankle and should not be
confused with fracture fragments. Three common ossicles include the os
trigonum (a separate ossicle posterior to the talus) or its fused variant, the Stieda
process; the os peroneum (within the peroneal longus tendon as it passes lateral
to the cuboid); and the os naviculare (also called accessory navicular, typically
proximal and medial to the navicular).
ANKLE TENDON INJURIES

Tendon injuries have been categorized into 6 types: tendinosis, peritendinosis,
tenosynovitis, entrapment, dislocation, and rupture.1,2 Achilles tendon tears and
tendonitis generally occur during athletic activity in middle-aged men.3
Conditions that predispose the tendon to injury include rheumatoid arthritis,
systemic lupus erythematosus, diabetes mellitus, and gout. The normal Achilles
tendon is a tapered structure with uniformly dark signal on all sequences. In
cross section, it has a C-shape that is normally concave toward the tibia but
becomes convex and thickened with tendinopathy or tears. Partial tears are
evident as thickening of the tendon with longitudinal bands of increased T1 and
T2 signal (Figure 10.3). Complete tendon tears are evident on MRI as
discontinuities with high T2 signal (Figure 10.4). Because the Achilles tendon
does not have a tendon sheath, tenosynovitis and frank fluid around the tendon
are not seen. However, soft-tissue edema in the soft tissues surrounding the
tendon may be present after an acute tear.
Tibialis posterior tendon injuries are frequently chronic, classically presenting
in mature women as a unilateral flatfoot deformity. The normal tibialis posterior
tendon traverses the ankle posterior and inferior to the medial malleolus and then
turns anteriorly along the sole of the foot to insert at the tuberosity of the
navicular bone, with multiple fibrous slips at the plantar aspects of the navicular
and medial cuneiform bones. The tibialis posterior provides dynamic support for
the medial longitudinal arch of the foot, and ruptures of it are therefore
associated with acquired, unilateral flatfoot deformity, often without a history of
trauma. On lateral weight-bearing radiographs, loss of the longitudinal arch may
be evident. On MRI, tears of the tibialis posterior are seen most frequently at or
within a few centimeters of its navicular insertion, distal to the medial malleolus.
The tendon will be thickened and have increased signal on T1 and T2 MRI, with
loss of continuity, surrounding edema, and fluid in the tendon sheath (Figure
10.5). Similar MRI findings without loss of continuity may indicate tibialis
posterior tendinosis.
•
FIGURE 10.3 Achilles tendinopathy and partial tear. Axial T2 MRI shows round
contour of distal Achilles tendon with heterogeneous high T2 signal (arrow).
•
FIGURE 10.4 Achilles tendon tear through the region of tendinosis. A, Sagittal PD
FS MRI shows a complete tear of the Achilles tendon with the retracted region filled
with fluid (*). The proximal (long arrow) and distal (short arrow) portions of the tendon
have abnormal high signal and swelling. B, Axial PD FS MRI through distal tendon
shows abnormal anterior convexity and prominent ovoid heterogeneity of the Achilles
tendon (arrow). The plantaris tendon (arrowhead) is anteromedial to the Achilles
tendon. C, Axial PD FS MRI through the level of the tear shows fluid filling the space
(*) left by the retracted Achilles tendon. The intact plantaris tendon is seen
anteromedially (arrowhead).
Tibialis anterior tendon injuries are most commonly seen in patients whose
athletic activities involve forced plantar flexion and ankle eversion; the
superficial location of the tendon also leaves it vulnerable to lacerations (Figure
10.6).
Peroneal tendon injuries usually occur during an acute injury. An os
peroneum, if present, may be fractured or may migrate proximally with the
retracting tendon, in particular with peroneal longus tears, and demonstrate
increased marrow signal on fluid-sensitive sequences. Tears of the peroneus
brevis typically occur at the level of the lateral malleolus as it makes its turn
anteriorly from behind the malleolus. Longitudinal splits are more common than
transverse tears (Figure 10.7), due to the posterior impingement of the longus on
the central posterior aspect of the peroneal brevis over time, giving rise to the
classic triangular “chevron sign” deformity of the peroneus brevis on transverse
images. Tears of the peroneus longus may accompany injuries of the peroneus
brevis but are less common and generally do not occur in isolation. Rare isolated
tears of the longus tend to occur at the level of the peroneal tubercle and cuboid
tunnel. Clues to injury include marrow edema in the lateral calcaneus or within a
hypertrophied peroneal tubercle. Lateral subluxation of the peroneal tendons and
even dislocation from behind the fibular malleolus can occur following injuries
to the SPR. The most common mechanism of SPR injury or tear is sudden
dorsiflexion of the foot with violent contraction of the peroneal muscles (ie,
most commonly seen in skiing injuries) with resultant lateral subluxation or
dislocation of the peroneal tendons from behind the fibular malleolus, causing
inability to evert the foot.4 Contributors to peroneal dislocations include
presence of an accessory peroneus quartus muscle, a shallow or flat
retromalleolar fibular groove, a calcaneus fracture with tendon impingement, or
concomitant peroneal tendon injury.5
•
FIGURE 10.5 Tibialis posterior tendon tear. Axial PD MRI shows tear within the
tibialis posterior tendon with edema surrounding the abnormal tendon (arrow).
FHL tendon injuries are rare and tend to occur in individuals who are
involved in continual plantar flexion hyperextension activities (ie, basketball
players or ballerinas) (Figure 10.8). In patients who have deficiencies of the
Achilles tendon, the FHL acts as the Achilles tendon and is at higher risk of
tendinopathy, partial or complete tear. In cases of complete tear, we extend the
axial imaging superiorly to locate the retracted tendon for surgical planning.
Although fluid around the flexor hallucis tendon is considered normal, fluid
within the tendon sheath that is greater than the volume of the tibiotalar joint
fluid in a symptomatic patient suggests stenosing tenosynovitis.
•
FIGURE 10.6 Tibialis anterior tendinopathy. A, Sagittal T1 MRI shows abnormal
thickening and signal heterogeneity within the partially torn tibialis anterior tendon
(arrow). B, Axial T2 FS MRI shows heterogeneous thickening of the tibialis anterior
tendon, consistent with tendinosis and partial tear (arrow).
•
FIGURE 10.7 Longitudinal tear of the peroneus brevis tendon. Axial T1 MRI shows
abnormal split morphology of the peroneus brevis tendon (arrow) with low signal in
the surrounding tendon sheath.
ANKLE LIGAMENT INJURIES

Lateral ankle sprains are very common and constitute as many as a fifth of all
sports-related injuries.6 Ankle inversion is the most common mechanism. The
ATFL is the most vulnerable of the 3 components of the lateral collateral
ligament and is the most frequently torn. Lateral ankle sprains usually follow a
predictable pattern of injury: The ATFL is torn first, then the calcaneofibular
ligament, and then the PTFL.7 The calcaneofibular ligament prevents widening
on inversion stress and is typically injured in conjunction with the ATFL (Figure
10.9). PTFL injury is rare with avulsion fracture of its posterior malleolar
attachment being more common. Lateral ankle sprains may be graded by the
number of ligaments involved (Grade 1 = 1 ligament, usually ATFL; Grade 2 = 2
ligaments, usually ATFL and calcaneofibular ligament; and Grade 3 = all 3
ligaments).
Medial ankle sprains involving the deltoid ligament typically with pronation-
eversion or rotational injuries. Deep deltoid ligament sprains are more common
than superficial sprains (Figure 10.10).8 Deltoid contusions (Grade 1 sprain),
particularly of the tibiotalar component, have been frequently associated with
inversion sprains.9 MR evaluation of deltoid ligament integrity is critical in the
setting of ankle fractures because it is a primary stabilizer of the ankle.
Associated findings may include lateral and syndesmotic ligament injuries and
lateral malleolar fractures, in particular Weber type B fractures.10 Deltoid
injuries can be associated with medial impingement syndromes and in chronic
medial instability. Chronic deltoid injury, with a thickened low-signal-intensity
ligament on all sequences, is common in patients with tibialis posterior tendon
dysfunction.11
Low-grade sprains of the ankle syndesmosis are more common than frank
tears and appear as heterogeneous high signal on MRI. Complete tears require
separation of the fibula from the tibia and should show abnormal fluid replacing
the normal structure in association with tibiofibular joint space widening; tears
of the anterior and posterior tibiofibular ligaments or fractures of their
attachments should also be present. Abnormal fluid signal intensity measuring
>12 mm within the distal tibiofibular articulation on coronal MRI suggests
syndesmotic disruption. In a study, a 5-fold increased risk of concomitant ankle
injury was noted in patients with syndesmotic injuries.12
•
FIGURE 10.8 Flexor hallucis longus strain in a 28-year-old woman with persistent
ankle pain superior to medial malleolus. A, Axial and B, sagittal PD FS MR
demonstrate edematous increased signal at the musculotendinous junction with focal
fluid, consistent with partial tear at the level of the posterior malleolus (white arrows).
•
FIGURE 10.9 Subacute ankle sprain in a 22-year-old woman who turned her ankle
badly. A, Axial PD FS MRI shows tear of the anterior talofibular ligament evidenced by
its absence and resultant distension of the ankle capsule (arrowheads). B, Coronal
PD FS MRI shows mild sprain of the calcaneal fibular ligament with high signal but
intact fibers (long arrow). There is a bone bruise of the talus (*). C, Coronal PD FS
MRI shows mild sprain of the posterior talofibular ligament (short arrow).
Injuries to the sinus tarsi ligaments can occur during inversion sprain giving
rise to nonspecific lateral ankle pain and hindfoot instability and should be
considered in the differential diagnosis for nonspecific lateral ankle pain in the
absence of other injuries. MR demonstrates resulting effacement or replacement
of sinus tarsi fat with high signal edema or fluid in the acute/subacute setting
(Figure 10.11).
•
FIGURE 10.10 Deltoid ligament sprain. Axial T2 FS MRI shows thickening of deep
deltoid ligament (*) with heterogeneous signal and loss of the normal striations.
Associated longitudinal split tear of the posterior tibialis tendon (PTT). There is also a
tear of the anterior talofibular ligament (white arrow). F, fibula; T, talus.
•
FIGURE 10.11 Stress reaction talus in a patient with 3-month history of midfoot pain
with repeated trauma. Sagittal T2 FS MRI shows edema in the distal talus without
fracture (black arrow) and sparing of the talar dome. Marked abnormal edema within
the dorsal talonavicular ligament (black arrowheads) and interosseous talocalcaneal
ligament (white arrowheads) of the sinus tarsi consistent with sprain. Note joint
effusion, subcutaneous edema, and edema in Kager fat pad (K). Case courtesy Dr
Jacob Mandell.
TRAUMATIC FRACTURES
Fractures demonstrate low signal linear abnormalities on both T1 and T2 with or
without accompanying edema (Figure 10.12). Acute injuries tend to have more
marrow edema than subacute or chronic injuries.
MRI may uncover missed or nondisplaced fractures in the setting of ankle
trauma, such as anterior process of the calcaneus or medial, lateral, or posterior
processes of the talus. Posterior process of the talus fracture fragments may be
difficult to distinguish from an os trigonum on radiographs, but the distinction
can be made on MRI by the presence of marrow edema.13 Bone bruises of the
talar dome, tibial plafond, or articular surfaces of the malleoli may be present
without corresponding radiographic or CT abnormality.
Acute, repetitive, or chronic inversion or compression injuries to the talus can
result in painful subchondral osteochondral lesions of the talar dome, most
common within the supralateral aspect, with or without a fracture fragment
(Figure 10.13). These are the most frequently missed fractures in inversion
injuries.6 MRI is the earliest method of detection, demonstrating early
subchondral edema even when radiographs are normal, and is useful for
detection and determination of stage for treatment planning and to assess
healing. The severity of osteochondral defects ranges from a cartilage injury
(stage 1), to an attached osteochondral fragment (stage 2), to a detached but
nondisplaced fragment (stage 3), to a detached and displaced fragment (stage 4),
and to secondary osteoarthritis (stage 5). Stages 3 and 4 are considered to be
unstable.14
Injuries to ossicles or sesamoids can occur and include contusion (increased
marrow edema on fluid-sensitive sequences), fracture (linear fracture line),
sclerosis from chronic injury to the vascular supply, and subluxation or
dislocation often in conjunction with tendon injuries to the tendons that they are
embedded in. A painful pseudoarticulation/synchondrosis may occur between
ossicles and native bone due to repetitive motion with edema on both sides of the
articulation with or without fluid within the synchondrosis (Figure 10.14).
IMPINGEMENT SYNDROMES
Anterior, posterior, and anterolateral impingement syndromes contribute to loss
of motion of the ankle joint. Anterior impingement is most common in young
athletes after repetitive forced dorsiflexion (ie, football, soccer, dancers,
baseball).15 The anterior distal tibia abuts the dorsal talar neck, is typically due
to osteophyte formation, and presents with anterior pain. Posterior impingement
refers to posterior ankle pain and limited plantar flexion due to the presence of
an os trigonum (isolated ossicle posterior to the talus) or prominent Stieda
process (posterior extension of the talus). It is seen that extreme repetitive
plantar flexion gives rise to a nutcracker impingement of the posterior soft
tissues. MRI findings include variations of bone edema or fracture of the os
trigonum or Stieda process, inferior distal tibia, or superior posterior calcaneus,
and associated posterior bursal edema/fluid. Accessory muscles can also
contribute to posterior impingement symptoms (Figure 10.15). Anterolateral
impingement is less common. It occurs in young individuals after injury to the
lateral ligaments (typically the ATFL) with resultant low-signal
hemorrhage/synovial scar tissue within the anterolateral gutter (between the
tibia, fibula, and talus) causing limitation of motion. More recently, anteromedial
impingement has been recognized following supination inversion injury and
repetitive microtrauma, leading to tearing of the anteromedial capsule,
thickening, and synovitis.15
•
FIGURE 10.12 Acute ankle fractures and bone bruises in a 52-year-old woman with
lateral ankle pain and negative radiographs. A, Coronal T2 FS MRI shows minimally
displaced lateral malleolar fracture (arrowhead). There is a bone bruise of the medial
malleolus (short arrow) and a sprain of the deep portion of the deltoid ligament (long
arrow). There is extensive soft-tissue swelling. B, Sagittal PD MRI shows oblique
lateral malleolar fracture (arrow). C, Sagittal T2 FS MRI shows large ankle effusion
(arrowhead) and bone bruise of the posterior malleolus (arrow).
•
FIGURE 10.13 Osteochondral lesions of the talar dome (different patients). A,
Coronal PD FS MRI shows a small osteochondral defect in the lateral talar dome. The
central fragment is detached and partially displaced from the dome of the talus
(arrow), and there is surrounding fluid. Subchondral bone marrow edema is also seen
in the lateral aspect of tibial plafond. B, Coronal T2 FS MRI shows focal marrow
edema at the lateral talar dome (arrow) and medial aspect of lateral malleolus.
STRESS REACTIONS AND STRESS FRACTURES

Stress injuries are common in the ankle and foot and radiographs may be
negative. MRI is generally preferred as the next step, rather than CT,
sonography, or nuclear imaging. Stress reaction is characterized as bone marrow
or periosteal edema on fluid-sensitive sequences without signal changes on T1-
weighted images, with true fracture demonstrating signal abnormalities on T1
and fluid-sensitive sequences with eventual fracture line. The most common
low-risk (better healing outcomes) stress fractures of the ankle include the
posteromedial tibia and the calcaneus (Figure 10.16), followed by the distal
fibula. High-risk stress fractures (prone to delayed union/nonunion) include the
medial malleolus, navicular, anterior tibial cortex, talus, and bases of the second
and fifth metatarsals.16
The most common stress fractures of the foot include the midneck to distal
neck of the second and third metatarsals (Figure 10.17) and diaphysis of the
second through fourth metatarsals (so-called march fractures because they are
common in marching military recruits), bases of the second and fifth metatarsals,
navicular, and hallux sesamoids (Figure 10.18).16 Navicular fractures tend to
occur in the central avascular central region of the bone, are typically vertical,
and occur in high-level running athletes (Figure 10.19).17 Cuneiform and cuboid
stress fractures are rare but tend to heal without complication (Figures 10.20 and
10.21).
•
FIGURE 10.14 Accessory navicular syndrome. Painful navicular synchondrosis
secondary to repetitive athletic injury. Axial PD FS MRI shows type II os naviculare (*)
with marrow edema on both sides of the synchondrosis. N, navicular.
•
FIGURE 10.15 Posterior ankle impingement in a young man with sports-related
posterior ankle pain. A, Axial T1 MRI at the level of the posterior malleolus shows
accessory or low-lying flexor hallucis longus muscle belly (*) and peroneus quartus
accessory muscle (arrow). B, Sagittal PD FS shows edema (*) where the muscles are
pinched between the bones during plantar flexion.
Stress fractures of the fifth metatarsal tend to involve the proximal

metadiaphysis, are typically transverse in nature, and occur more distal than
traumatic avulsion injuries of the metatarsal base. Proximal diaphyseal fractures
have increased risk of poor healing due to the vascular watershed anatomy of
this region.18 The classic Jones fracture occurs at the proximal metaphysis.
Whereas periosteal reaction is common in occult metatarsal fractures, it is
uncommon in tarsal bones.
LISFRANC INJURY
The Lisfranc joint refers to the hindfoot-midfoot articulation, including the
tarsometatarsal (TMT), intermetatarsal, and small intertarsal joints. Lisfranc
fractures-dislocations are usually the result of high-energy trauma such as car
crashes (see chapter 3), while Lisfranc sprains (also called midfoot sprains)
typically result from low-energy injuries. Radiography and CT should be
obtained first; MRI has a limited role in problem-solving when radiography and
CT leave questions. Undiagnosed Lisfranc sprains can lead to chronic instability
and early osteoarthritis. The bones of the Lisfranc joint form the osseous
foundation of the transverse and longitudinal arches. The Lisfranc ligament
attaches the medial cuneiform to the base of the second metatarsal and has
separate dorsal, interosseous, and plantar components (Figure 10.22).19–21 There
are highly variable arrangements of ligaments that attach the second through
fifth metatarsal bases and the 3 cuneiforms to their neighbors. The first TMT has
a dorsal and plantar ligament, but there is no ligament between the first
metatarsal and the second metatarsal. On MRI, low-energy Lisfranc injuries may
manifest as bone bruises in the TMT region, increased signal within the
ligaments, ligament elongation, or periligamentous edema (Figure 10.23).22,23
Small avulsion fractures may be difficulty to see on MRI and are generally more
apparent on CT. Three stages of low-energy Lisfranc sprains have been
described. Stage I has a low-grade sprain of the Lisfranc ligament with intact
stability. Stage II has elongation or tear of the Lisfranc ligament with intact
plantar ligaments, possibly with instability. Stage III has tears of both Lisfranc
and plantar ligaments with instability.22
•
FIGURE 10.16 Stress fracture calcaneus in a runner with heel pain, who is not
responding to treatment. A, Axial T1 MRI shows dark irregular fracture line (arrow)
through posterior calcaneus. B, Sagittal T2 FS MRI shows the fracture (arrow) with
extensive associated calcaneal bone marrow edema.
•
FIGURE 10.17 Stress fracture of the third metatarsal shaft. A, Short-axis PD FS
MRI shows marrow edema in the third metatarsal shaft with surrounding soft-tissue
edema (arrow). B, Long-axis PD FS MRI shows extensive marrow and soft-tissue
edema at the distal third metatarsal shaft (arrow). C, Long-axis T1 MRI shows
thickened cortex (arrowhead) and nondisplaced fracture line.
TURF TOE
The plantar capsuloligamentous complex of the great toe includes the MTP joint,
as well as the articulation of the medial and lateral sesamoids (also called the
tibial and fibular sesamoids) with the plantar surface of the great toe. Each
sesamoid has its own articular facet, separated from the other by a bony ridge
called the crista. The sesamoids are located within the medial and lateral tendons
of the flexor hallucis brevis, which both insert on the proximal phalanx. The
sesamoids are stabilized to the metatarsal head and proximal phalanx by
collateral ligaments and to each other by the intersesamoid ligament. The plantar
plate extends from the intersesamoid ligament to the proximal phalanx. The FHL
tendon courses between the sesamoids, superficial to the intersesamoid ligament,
to the distal phalanx. Not all of these structures are separately identifiable on
routine MRI (Figures 10.24 and 10.25).
•
FIGURE 10.18 Stress fracture of the third metatarsal base in a 33-year-old woman
training for marathon. A, Short-axis, B, long-axis, and C, sagittal PD FS MRI
demonstrate edema localized to the third metatarsal base (arrows) without injury to
the adjacent bones. Surrounding soft-tissue edema can also be seen.
•
FIGURE 10.19 Stress reaction of the navicular. A, Sagittal and B, long-axis PD FS
MRI show high signal within the navicular (N). C1, medial cuneiform.
•
FIGURE 10.20 Stress fracture of the midfoot in a 27-year-old runner with midfoot
pain. A, Long-axis PD FS MRI in the plane of the metatarsals shows edema in the
medial cuneiform (arrow), indicating stress fracture. There is an associated sprain of
the Lisfranc ligament. B, Short-axis PD FS MRI shows the stress fracture in the upper
portion of the medial cuneiform (arrow), with sparing of the inferior portion (*). C,
Sagittal PD FS MRI shows a bipartite medial cuneiform, an anatomic variant, with
marrow edema in the superior portion (arrow) but not in the inferior portion (*). 1MT,
first metatarsal.
•
FIGURE 10.21 Stress fracture of the cuboid. A, Sagittal and B, long-axis PD FS
MRI show high signal within the cuboid (arrows), consistent with stress fracture. M4,
fourth metatarsal base.
•
FIGURE 10.22 Lisfranc ligament anatomy. A, Short-axis PD MRI shows the 3
components of the Lisfranc ligament: dorsal ligament (long arrow), interosseous
ligament (short arrow), and plantar ligament (arrowhead). M1, first metatarsal; M2,
second metatarsal. B, Long-axis T2 FS MRI shows interosseous Lisfranc ligament
(white arrow) extending obliquely from the medial cuneiform to the second metatarsal.
C1, medial cuneiform; C2, middle cuneiform; N, navicular.
FIGURE 10.23 • Lisfranc joint sprain. A, Short-axis PD FS MRI shows
heterogeneous increased signal in the dorsal (black arrows) and plantar components
(black arrowheads) consistent with high-grade sprain. There is a bone bruise at the
base of the medial cuneiform (*). Distal aspect of the peroneus longus tendon is seen
as fibrillated band (white arrow). B, Long-axis PD FS MRI demonstrates abnormal
diffuse increased signal within the Lisfranc ligament (arrow) with soft tissue. C1,
medial cuneiform; M1, first metatarsal.
•
FIGURE 10.24 Normal anatomy of the plantar capsuloligamentous complex of the
first MTP joint. A, Sagittal and B, short-axis PD MR images. Sesamoid phalangeal
ligament (white arrowheads), metatarsosesamoid ligament (black arrowheads),
intersesamoidal ligament, collateral ligaments (CL), joint capsule, tendinous
insertions, plantar portions of the abductor and adductor hallucis tendons, flexor
hallucis longus (FHL) (runs between the sesamoids (S) to insert on the distal
phalanx), and the plantar plate. The plantar plate originates from the metatarsal head
(MT) and inserts on the base of the proximal phalanx; ossific structures include the
volar metatarsal head crista (C), volar base of the proximal phalanx (PP), and the
adjacent medial (MS) and lateral sesamoids (LS) embedded in the flexor hallucis
brevis tendon heads.
Turf toe, or plantar hyperextension injury to the first MTP joint, takes its
name from a description of the injury in football players who played on artificial
turf.24 The mechanism is a planted, dorsiflexed first MTP that is axially loaded
through the first metatarsal shaft. The injury consists of varying degrees of soft-
tissue, chondral, and ossific damage to the plantar capsuloligamentous complex,
which connects the first metatarsal head, proximal phalanx, and medial and
lateral sesamoids.25 Three grades of severity have been described: low-grade
sprain without tear; partial tear; and complete tear with gross instability (Figure
10.26). The injuries typically occur between the sesamoids and the proximal
phalanx and may include the plantar plate tear, sesamoid fracture, or traumatic
diastasis of a bipartite sesamoid.26,27 Proximal phalangeal avulsion fractures may
be seen in conjunction with ligamentous injury. Surgical treatment is sometimes
required for traumatic hallux valgus deformity, chondral injury, loose intra-
articular bodies, retracted or diastatic sesamoids, or failed conservative
therapy.28
FIGURE 10.25 • Anatomic drawing of the normal plantar capsuloligamentous
complex first metatarsophalangeal joint. Courtesy Michael Richardson, MD.
•
FIGURE 10.26 Turf toe from soccer injury. A, Sagittal T2 FS MRI of the medial side
of the first metatarsophalangeal (MTP) joint demonstrates high-signal intensity tear of
the proximal phalangeal sesamoid ligament at sesamoid attachment (white arrow);
fluid in plantar plate between metatarsal head (MT), proximal phalanx (PP), and
distracted bipartite medial sesamoid (S). Sprain of the metatarsosesamoid ligament at
the base of sesamoid (white arrowhead) with strain (increased signal intensity) in
adjacent muscle. B, Sagittal T2 FS MRI of the lateral side of the first MTP joint. Intact
phalangeal sesamoid ligament (arrow) attached to edematous lateral sesamoid
(arrowhead). Bone contusion of the MT. C, Short-axis PD FS MRI depicts complete
tear of the intersesamoid ligament (white arrow) creating an increased gap between
the medial sesamoid and the laterally displaced flexor hallucis longus tendon (F) with
adjacent edematous lateral sesamoid (arrowhead). Edema within the expected region
of the medial collateral ligament (short white arrows) is consistent with partial tear. C,
Crista of the first metatarsal head.
References
1. Trevino S, Baumhauer JF. Tendon injuries of the foot and ankle. Clin Sports Med. 1992;11:727–739.
2. Teitz CC, Garret WE, Miniaci A, Lee MH, Mann RA. Tendon problems in athletic individuals. J Bone
Joint Surg Am. 1997;79:138–152.
3. Prescott JW, Yu JS. The aging athlete: part 1: “Boomeritis” of the lower extremity. AJR Am J
Roentgenol. 2012;199:W294–W306.
4. Rosenberg ZS, Bencardino J, Astion D, Schweitzer ME, Rokito A, Sheskier S. MRI features of chronic
injuries of the superior peroneal retinaculum. AJR Am J Roentgenol. 2004;181:1551–1557.
5. Wong-Chung J, Marley WD, Tucket A. O’longain DS. Incidence and recognition of peroneal tendon
dislocation associated with calcaneal fractures. Foot Ankle Surg. 2015;21(4):254–259.
6. Rosenberg ZS, Beltran J, Bencardino JT. MR imaging of the ankle and foot. RadioGraphics.
2000;20(Spec No):S153–S179.
7. Jibri A, Mukherjee K, Kamath S, Mansour R. Frequently missed findings in acute ankle injury. Semin
Musculoskelet Radiol. 2013;17(4):416–428.
8. Mengiardi B, Pinto C, Zanetti M. Medial collateral ligament complex of the ankle: MR imaging
anatomy and findings in medial instability. Semin Musculoskelet Radiol. 2016;20(1):91–103.
9. Klein MA. MR imaging of the ankle: normal and abnormal findings in the medial collateral ligament.
AJR Am J Roentgenol. 1994;162:377–383.
10. Hintermann B, Knupp M, Pagenstert GI. Deltoid ligament injuries: diagnosis and management. Foot
Ankle Clin. 2006;11(3):625–637.
11. Chhabra A, Subhawong TK, Carrino JA. MR imaging of deltoid ligament pathologic findings and
associated impingement syndromes. RadioGraphics. 2010;30(3):751–761.
12. Schoennagel BP, Karul M, Avenesov M, et al. Isolated syndesmotic injury in acute ankle trauma:
comparison of plain film radiography with 3T MRI. Eur J Radiol. 2014;83(10):1856–1861.
13. Bonvin F, Montet X, Copercin IM, Martinoli C, Bianchi S. Imaging of fractures of the lateral process of
the talus, a frequently missed diagnosis. Eur J Radiol. 2003;47(1):64–70.
14. Hepple S, Winson IG, Glew D. Osteochondral lesions of the talus: a revised classification. Foot Ankle
Int. 1999;20(12):789–793.
15. Robinson P, White L. Soft tissue and osseous impingement syndromes of the ankle: role of imaging in
diagnosis and management. RadioGraphics. 2002;22:1457–1471.
16. Mandell JC, Khurana B, Smith SE. Stress fractures of the foot and ankle, part 2: site specific etiology,
imaging, and treatment, and differential diagnosis. Skeletal Radiol. 2017;46(9):1165–1186.
17. Gross CR, Nunley JA. Navicular stress fractures. Sports Topical Review. Foot Ankle Int.
2015;36(9):1117–1122.
18. Smith JW, Arnoczky SP, Hersh A. The intraosseous blood supply of the fifth metatarsal: implications
for proximal fracture healing. Foot Ankle. 1992;13(3):143–152.
19. Siddiqui NA, Galizia MS, Almusa E, Omar IM. Evaluation of the tarsometatarsal joint using
conventional radiography, CT and MR imaging. RadioGraphics. 2014;34(2):514–531.
20. Llopis E, Carrascoso J, Iriarte I, De Prado Serrano M, Cerezal L. Lisfranc injury imaging and surgical
management. Semin Musculoskelet Radiol. 2016;20(2):139–153.
21. Castro M, Melão L, Canella C, et al. Lisfranc joint ligamentous complex: MRI with anatomic
correlation in cadavers. AJR Am J Roentgenol. 2010;195(6):W447–W455. doi:10.2214/AJR.10.4674
[PMID:21098178].
22. Nunley JA, Vertullo CJ. Classification, investigation, and management of midfoot sprains: Lisfranc
injuries in the athlete. Am J Sports Med. 2002;30(6):871–878.
23. Tafur M, Rosenberg ZS, Bencardino JT. MR imaging of the midfoot including Chopart and Lisfranc
joint complexes. Magn Reson Imaging Clin N Am. 2017;25(1):95–125. doi:10.1016/j.mric.2016.08.006.
24. Bowers Jr KD, Martin RB. Turf-toe: a shoe-surface related football injury. Med Sci Sports. 1976;8:81.
25. Crain JM, Phancao JP. Imaging of turf toe. Radiol Clin North Am. 2016;54(5):969–978.
26. Anderson RB. Turf toe injuries of the hallux metatarsophalangeal joint. Tech Foot Ankle Surg.
2002;1:102–111.
27. Nery C, Baumfeld D, Umans H, Yamada AF. MR imaging of the plantar plate: normal anatomy, turf toe,
and other injuries. Magn Reson Imaging Clin N Am. 2017;25(1):127–144.
doi:10.1016/j.mric.2016.08.007.
28. Mason LW, Molloy AP. Turf toe and disorders of the sesamoid complex. Clin Sports Med.
2015;34(4):725–739.
1. Which of the following is the most commonly injured ankle ligament?

A. Anterior talofibular ligament
B. Posterior talofibular ligament
C. Anterior tibiofibular ligament
D. Posterior tibiofibular ligament
2. Which type of peroneal tendon tear is most commonly seen on MRI?

A. Distal avulsion of the peroneus longus
B. Segmental tear of the peroneus brevis
C. Split tear of the peroneus brevis
D. Combined tears of both peroneus longus and brevis
3. Which of the following injuries of the Achilles tendon is the least common?
A. Tendinosis
B. Tenosynovitis
C. Partial tear
D. Complete tear
4. Tendon dislocation is most closely associated with injuries of which tendon?

A. Achilles
B. Tibialis anterior
C. Peroneus brevis
D. Extensor hallucis longus
Answer to Chapter Self-assessment Questions

1. A The anterior talofibular ligament is the most common ankle sprain.
2. C Split tear of the peroneus brevis is the most common peroneal tendon
injury.
3. B Tenosynovitis of the Achilles tendon never occurs because the Achilles
tendon does not have a synovial sheath.
4. C Dislocation of the peroneal tendons from behind the lateral malleolus may
occur with injuries of the SPR.
11
Imaging Basics of Bone Tumors
Felix S. Chew
Bone tumors are an important concern in musculoskeletal radiology, and a

systematic approach is necessary.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging basics of bone tumors, the learner
will be able to
2. describe radiologic features,
3. develop and narrow a differential diagnosis, and
4. summarize relevant concepts and knowledge for the following topics: bone tumor epidemiology,
cardinal principle of diagnosis, patient factors, location of lesion, rate of growth, tissue
characterization, staging, treatment, bone metastases, and the solitary bone lesion.
INCIDENCE
Malignant primary bone tumors are rare, with about 3300 new cases reported
annually in the United States.1 That is fewer than 1 new case per decade per
radiologist. In adults, a bone malignancy is much more likely to be a metastasis
or multiple myeloma than a primary sarcoma. The radiologist’s primary task is
to determine if a bone lesion is actually present. Once confirmed, the radiologist
should determine whether the lesion is aggressive or nonaggressive, and only
then speculate as to which specific entity it might be. Once the diagnosis is
suspected or confirmed, patients with aggressive primary bone lesions are
usually referred to academic medical centers with special expertise, and a biopsy
is always part of the evaluation.
CARDINAL PRINCIPLE
The radiologic appearance of a bone lesion reflects the underlying pathology and
its interplay with the host bone.2 The standard radiologic approach addresses 4
issues: (1) patient factors, especially age; (2) location within the skeleton and
within the involved bone; (3) rate of growth or aggressiveness; and (4) tissue
characterization from specific features such as mineralization.3,4 Sometimes a
specific diagnosis can be made, but oftentimes not. For some musculoskeletal
lesions, a combination of pathology and radiology may be necessary to provide a
definitive diagnosis.
PATIENT FACTORS
Most bone lesions tend to affect particular age groups, and their frequency varies
with age (Table 11.1).1,5–7 Many bone lesions have a broad age range. Most bone
lesions are more common in males. A few precursor conditions increase the risk
of developing a bone malignancy, including osteochondromatosis,
enchondromatosis, and Paget disease.
LOCATION OF LESION
The location of a lesion within the skeleton and within the involved bone may
have considerable differential diagnostic significance (Tables 11.2 and 11.3).5–7
CT or MRI may help identify the site of origin when radiographs are equivocal.
RATE OF GROWTH
The rate of growth of a lesion is classified according to the type of bone
destruction and the type of bone proliferation in response to the presence of the
lesion.8,9 Bone destruction occurs when normal bone tissue is replaced by
lesional tissue. Bone destruction is described as geographic when it is confined
to a focal area, forming a single hole in the bone (Figure 11.1). The demarcation
between the lesion and normal unaffected bone can be sharp or gradual. Bone
destruction is described as moth-eaten when there are multiple medium-sized
holes with irregular edges randomly distributed in the area of involvement
(Figure 11.2). It is described as permeated when the multiple holes are so small
that the overall outline of the bone may remain intact in the presence of
extensive destruction (Figure 11.3). In moth-eaten and permeated destruction,
the transition between normal and abnormal bone is usually gradual.
Proliferative bone is a reaction to the lesion by the host bone. This reaction can
be endosteal, within the bone, or periosteal, on the cortical surface. A sclerotic
rim is a layer of dense endosteal reactive bone surrounding the lesion and
separating it from normal adjacent bone (Figure 11.4). A sclerotic rim implies
that the growth rate of the lesion is slow enough for new bone to form around it
and confine it. An expanded cortical shell is a layer of periosteal new bone that
confines a lesion that has already destroyed the cortex and expanded beyond the
original contour of the bone (Figure 11.5). The periosteal new bone is formed as
the endosteal surface of the cortex is destroyed; the faster the cortical destruction
and expansion of the lesion, the thinner is the cortical shell. An expanded shell
may have ridges or trabeculations on the endosteal surface, reflecting an uneven
growth rate. Nodules of tumor have grown more rapidly beneath the thinner
areas of bone and less rapidly where the trabeculations are located. True bony
septations that divide a lesion into compartments are rare. If a lesion expands so
rapidly that the periosteal bone response cannot keep up, a shell will not be
visible. Mottled sclerosis, scattered throughout cancellous bone adjacent to a
lesion, suggests disorganized reactive bone formation in the presence of an
aggressive, fast-growing lesion. Cortical penetration by an intramedullary lesion
is indicative of an aggressive process (Figure 11.6) typically apparent by the
presence of a soft-tissue mass. Periosteal reaction may also indicate cortical
penetration. Layers of periosteal reaction may be caused by cortical penetration
of the lesion into the subperiosteal region (Figure 11.7). A sunburst periosteal
reaction or streaks of periosteal new bone indicate penetration with reactive
bone-forming periosteum being carried along by an expanding lesion (Figure
11.8). An interrupted layer of bone at the edge of a lesion that has expanded
beyond the periosteum may be present, the so-called Codman triangle. The
presence of a Codman triangle at the margin of a destructive lesion is a strong
indication of aggressiveness.
Table 11.1 MOST FREQUENTLY ENCOUNTERED TYPES OF PRIMARY MALIGNANT BONE

TUMORS AT VARIOUS AGES
0-9 y 10-19 y 20-29 y 30+ y

Ewing Osteosarcoma Osteosarcoma Myeloma
sarcoma
Osteosarcoma Ewing sarcoma Chondrosarcoma Chondrosarcoma
Primary Primary Ewing sarcoma Osteosarcoma
lymphoma lymphoma
Primary Primary
lymphoma lymphoma
MFH/fibrosarcoma Chordoma
MFH/fibrosarcoma
Based on Unni KK, Inwards CY. Dahlin’s Bone Tumors: General
Aspects and Data on 10,165 Cases. 6th ed. Philadelphia: Lippincott
Williams & Wilkins; 2010.
For each age range, the tumor types are listed in order of frequency
and account for approximately 90% or more of the primary tumors.
MFH, malignant fibrous histiocytoma (now called undifferentiated high-
grade pleomorphic sarcoma).
Table 11.2 TYPICAL LONGITUDINAL LOCATIONS OF SOLITARY BONE LESIONS
Epiphysis Metaphysis Diametaphysis Diaphysis

Chondroblastoma Osteochondroma Benign fibrous Ewing
lesions sarcoma
Eosinophilic Osteosarcoma Malignant fibrous Myeloma
granuloma lesions
Giant cell tumor Enchondroma Chondromyxoid Lymphoma
fibroma
Subchondral cyst Chondrosarcoma Simple bone cyst
Brodie abscess Osteoid osteoma
Clear cell Osteoblastoma
chondrosarcoma
Table 11.3 TYPICAL TRANSVERSE LOCATIONS OF SOLITARY BONE LESIONS
Medullary Cavity Cortex Juxtacortical

Conventional Cortical osteoid Osteochondroma
osteosarcoma osteoma
Medullary Fibrous cortical Periosteal chondroma
chondrosarcoma defect
Ewing sarcoma Adamantinoma Parosteal
osteosarcoma
Myeloma Exostotic
chondrosarcoma
Lymphoma
Giant cell tumor
Enchondroma
Simple bone cyst
Nonossifying fibroma
•
FIGURE 11.1 Geographic bone destruction (arrow) in proximal femur (giant cell
tumor).
•
FIGURE 11.2 Moth-eaten bone destruction (multiple myeloma). A, Humerus. B,
Skull.
•
FIGURE 11.3 Permeated bone destruction (arrow) in anterior femoral cortex with
soft-tissue extension (metastasis). A, Lateral radiograph. B, Sagittal T1 FS Gd MRI.
The rate of growth reflects the biologic aggressiveness of the lesion and can
be assigned a radiologic grade. The grading system devised by Lodwick at the
Armed Forces Institute of Pathology (AFIP) may be used by subspecialists
(Table 11.4).8,9 Growth rate I-A is geographic destruction with a complete
sclerotic margin and partial or no cortical destruction; the cortex may be
expanded by up to 1 cm (see Figure 11.4). Growth rate I-B is geographic
destruction with either no sclerotic rim or cortical expansion greater than 1 cm
(Figure 11.9). Growth rate I-C is geographic destruction with complete cortical
penetration. Growth rate II is geographic destruction combined with moth-eaten
or permeated destruction, or both (see Figure 11.6). Growth rate III is moth-
eaten destruction with or without permeated destruction only (see Figure 11.2).
Higher-grade growth rates may have features of lower-grade growth rates, but
not vice versa. Lesions with growth rate I-A are low grade and nonaggressive,
lesions with growth rate I-B or I-C are medium grade and moderately
aggressive, and lesions with growth rate II or III are high grade and very
aggressive. The important radiologic distinction is between growth rate 1-A
(nonaggressive) and all the others (aggressive).
•
FIGURE 11.4 Sclerotic rim (arrow) around lesion in proximal tibia (nonossifying
fibroma).
•
FIGURE 11.5 Expanded cortical shell in fifth metacarpal (osteoblastoma).
•
FIGURE 11.6 Geographic destruction and cortical penetration with Codman triangle
(arrow) in distal femur (osteosarcoma). There is a medial soft-tissue mass
(arrowheads) with faint sunburst periosteal reaction.
•
FIGURE 11.7 Layers of periosteal reaction with Codman triangle (osteosarcoma).
TISSUE CHARACTERIZATION
Many primary musculoskeletal tumors form an extracellular matrix with
distinctive radiologic characteristics determined by the relative proportions of
cells and matrix and the composition and mineralization of the matrix.2 Types of
tumor matrices include osteoid (osseous), chondroid (cartilaginous), myxoid
(proteinaceous), and fibrous (collagenous). Identifying the type of matrix often
suggests a specific diagnosis (Table 11.5). The pattern of mineralization on
radiographs, the attenuation on CT, and the signal on MRI may be helpful in
identifying a tumor matrix. Dense homogeneous mineralization is typical of an
osteoid matrix, formed by benign and malignant bone-forming lesions (Figure
11.10). Alternatively, an osteoid matrix may have a ground-glass or intermediate
pattern of matrix mineralization. An osteoid matrix is not always mineralized;
therefore, the lack of densely mineralized matrix does not rule out the possibility
of an osteoid-forming lesion. A nonmineralized osteoid matrix may have
attenuation on CT similar to muscle and often has low signal on both T1- and
T2-weighted MRI.
•
FIGURE 11.8 Sunburst periosteal reaction (osteosarcoma). A, Anteroposterior
radiograph. B, Axial CT.
Table 11.4 RADIOLOGIC GRADING OF DESTRUCTIVE BONE LESIONS
AFIP Simplified
System Defining Characteristics System
I-A Geographic destruction; well-defined lucent Low grade;
destruction with sclerotic margin; cortex nonaggressive
expanded up to 1 cm
I-B Geographic destruction; well-defined lucent Medium
destruction without sclerotic margin or cortex grade;
expanded >1 cm moderately
aggressive
I-C Geographic destruction; complete cortical
penetration with ill-defined margin
II Geographic destruction combined with moth- High grade;
eaten or permeated destruction, middle-sized very
holes in bone with irregular poorly defined aggressive
contours
III Moth-eaten or permeated destruction only,
numerous elongated slotted holes parallel to
long axis
Based on Hudson TM. Radiologic-Pathologic Correlation of
Musculoskeletal Lesions. Baltimore: Williams & Wilkins; 1987.
AFIP, Armed Forces Institute of Pathology.
•
FIGURE 11.9 Geographic destruction with no sclerotic margin in distal radius (giant
cell tumor); a pathologic fracture is present. A, Radiograph. B, Coronal CT.
Table 11.5 MATRIX MINERALIZATION IN BONE TUMORS
Intermediate
Osteoid Matrix Chondroid Matrix Matrix
Benign Osteoid Enchondroma Fibrous dysplasia
osteoma
Osteoblastoma Osteochondroma Osteoblastoma
Bone island Periosteal chondroma
Osteoma Chondroblastoma
Chondromyxoid
fibroma
Malignant Osteosarcoma Chondrosarcoma Osteosarcoma
•
FIGURE 11.10 Mineralized osteoid matrix (osteosarcoma). A, Anteroposterior
radiograph. B, Coronal T1 FS Gd MRI.
Calcified rings and arcs, dense punctate calcifications, and flocculent

calcifications (small, loosely aggregated masses) are patterns of mineralization
of a chondroid matrix (Figures 11.11–11.13), formed by benign and malignant
cartilage-forming lesions. The rings-and-arcs configuration of mineralization
corresponds to calcification and ossification around the periphery of
cartilaginous lobules. A chondroid matrix that is not mineralized typically has
attenuation on CT that is lower than muscle but greater than water. On MRI, a
chondroid matrix has low signal on T1-weighted images and high signal on T2-
weighted images, similar to hyaline cartilage. A localized change in the character
of tumor matrix from mineralized to nonmineralized may indicate a focus of
higher-grade tumor cells.
A myxoid matrix may be formed by benign and malignant cartilage-forming
tumors and by other benign and malignant mesenchymal tumors, including
chordomas. A myxoid matrix generally does not mineralize and typically has
attenuation on CT that is lower than muscle and greater than water. On MRI, a
myxoid matrix has high T2 signal, presumably due to its high water content, and
variable T1 signal, presumably due to its variable protein content.
Lesions that form a fibrous matrix range from densely cellular fibrous tissue
to myxoid tissue, often within the same lesion. A fibrous matrix typically does
not mineralize. On CT, a fibrous matrix has variable, nonspecific attenuation,
depending on its composition. On MRI, a fibrous matrix has variable,
nonspecific signal, also depending on its composition. Fibrous dysplasia
characteristically has the intermediate pattern of mineralization (ground-glass
appearance). However, this appearance results from the presence of dysplastic,
microscopic bone spicules rather than mineralization of the fibrous matrix itself.
On radiographs, the ground-glass appearance may be difficult to recognize: The
lesion is denser than the marrow space but less dense than the cortical bone; CT
is often helpful in identifying the matrix (Figure 11.14).
A lesion with no mineralization will have either a matrix that is not
mineralized or no matrix at all. Lesions without a matrix may be densely cellular
(eg, Ewing sarcoma, lymphoma, myeloma), or they may be acellular (eg, bone
cyst) (see Figure 11.1). MRI may be diagnostic when a nonaggressive lesion can
be demonstrated to be fluid filled and therefore cystic.
•
FIGURE 11.11 Rings-and-arcs cartilage matrix mineralization (chondrosarcoma). A,
Lateral radiograph. B, Axial CT shows the lobular morphology of the tumor and the
calcifications.
•
FIGURE 11.12 Flocculent cartilage matrix mineralization (enchondroma).
•
FIGURE 11.13 Punctate cartilage matrix mineralization (enchondroma).
STAGING
Staging requires anatomic delineation of the tumor and the involvement of
surrounding tissue. The anatomic relationship of the lesion to all surrounding
structures, anatomic compartments, and neurovascular bundles is typically
established by MRI without and with contrast. Chest CT is the standard
screening examination for lung metastases; a radionuclide bone scan can help
characterize the activity of a lesion (Figure 11.15) and identify other skeletal
lesions. PET and PET/CT may also be used for characterization and
identification of metastases.
The Musculoskeletal Tumor Society surgical staging system (Enneking
staging system) for primary musculoskeletal tumors is based on the biologic
grade, the anatomic setting of the tumor, and the presence or absence of
metastases.10–12 Benign lesions have 3 stages, designated by Arabic number, that
are related to biologic and radiographic grade. Latent lesions (stage 1) are
associated with AFIP grade I-A (see Table 11.4); active lesions (stage 2) are
associated with grade I-B; and aggressive lesions (stage 3) are associated with
grade I-C. Malignant lesions have 3 stages designated by Roman numerals.
Stage I lesions are low-grade malignancies, stage II lesions are high-grade
malignancies, and stage III lesions have metastases. Malignant lesions are
associated with radiographic grades II and III. An additional letter designation of
A or B reflects the anatomic setting. Stages IA and IIA are intracompartmental
lesions in which the tumor is confined within a natural anatomic barrier to tumor
growth such as cortical bone, articular cartilage, major fascial septa, or joint
capsule. Stages IB and IIB are extracompartmental lesions, in which the lesion
has expanded beyond the confines of a single anatomic compartment, such as a
bone lesion that has penetrated the cortex and extended in the soft tissues.
•
FIGURE 11.14 Intermediate (ground-glass) mineralization (arrow) of matrix (fibrous
dysplasia), in the proximal tibia shown on coronal CT.
•
FIGURE 11.15 Osteosarcoma in a 44-year-old woman with large left distal femur
mass. A, Anterior Tc-99m radionuclide bone scan shows large region of increased
activity in distal femoral mass. B, Coronal T1 FS Gd MRI shows the large distal
femoral lesion with extension into the soft tissues.
Table 11.6 AJCC PROGNOSTIC STAGE GROUPS FOR PRIMARY BONE TUMORS
(EXCLUDING PELVIS AND SPINE)
Stage Grade Tumor Size Metastases

Up to 8 cm
IA More than 8 cm or noncontiguous
IB Low in primary site None
IIA Up to 8 cm
IIB High More than 8 cm
III Noncontiguous in primary site
IVA Pulmonary only
IVB Any Any Nonpulmonary
Based on Amin MB, Edge S, Greene F, et al, eds. AJCC Cancer
Staging Manual. 8th ed. New York: Springer; 2017:471–486.
The current AJCC system for prognostic stage groups diverges from the
Musculoskeletal Tumor Society system by applying only to primary bone
sarcomas, by excluding lesions of the pelvis and spine, and by using tumor size
and multifocality rather than intra- and extracompartmental localization to define
4 stages (Table 11.6).13 Small tumors are likely to be intracompartmental and
large tumors are likely to be extracompartmental, so there may not be much
practical difference. Some oncologic surgeons use only 2 stages: localized and
metastatic.
TREATMENT
Many benign lesions do not require treatment; others may be treated with
curettage or simple excision. Aggressive or malignant lesions usually require
both local and systemic therapy. Neoadjuvant and adjuvant therapies—including
radiation therapy, chemotherapy, and immunotherapy—are aimed at reducing
tumor bulk before surgery and eliminating residual tumor and subclinical
metastases after surgery. After the initiation of therapy, imaging may be used to
monitor the response and to screen for complications or recurrences (Figures
11.16–11.18).
For bone lesions that have undergone curettage with bone or cement grafting,
MRI is commonly used to evaluate the postsurgical site for recurrences (Figure
11.19). Radiographs or CT using a metal artifact reduction algorithm can be
useful for monitoring the treated area of bone for periprosthetic fracture,
infection, and graft incorporation. In cases where metal artifact is overwhelming,
Doppler ultrasound can evaluate the surrounding soft tissues for tumor
recurrence. PET is becoming progressively more utilized for tumor surveillance
in cases where large amounts of metal degrade CT and MRI (Figure 11.20).
METASTASES
Metastases to the lungs are common in patients with musculoskeletal sarcomas.
The lung lesions often have a cannonball morphology. The pulmonary
metastases of matrix-forming bone tumors may also form a similar matrix
(Figure 11.21). Musculoskeletal malignancies also metastasize to other bones
and soft tissues. The metastatic lesions generally resemble the primary lesions
(Figure 11.22).
•
FIGURE 11.16 Ewing sarcoma in the proximal femur. A, At presentation, there is
permeated destruction, layered periosteal reaction, and a large soft-tissue mass. B,
One year later, after radiation therapy, the mass has regressed and reactive bone is
present.
•
FIGURE 11.17 Soft-tissue sarcoma with the expected posttreatment changes. A,
Axial T2 FS MRI before surgery shows a large mass (arrow) in the anterior
compartment with high signal regions of necrosis. B, Axial T2 FS MRI 3 months after
surgery shows resection of the mass with a small seroma (arrow) at the surgical site.
The remaining quadriceps musculature (Q) shows increased signal from denervation
atrophy. C, Axial T1 FS Gd MRI shows modest enhancement around the periphery of
the seroma (arrow).
•
FIGURE 11.18 Recurrent soft-tissue sarcoma. A, Axial T1 MRI shows a lesion
(arrow) with intermediate in the anterior subcutaneous tissues of the proximal thigh.
The marker has been placed on the incision scar from previous surgery. B, Axial T2
FS MRI shows heterogeneous high signal within the lesion. C, Axial T1 FS Gd MRI
shows heterogeneous enhancement in the lesion.
•
FIGURE 11.19 Recurrent giant cell tumor. A, Posteroanterior radiograph shows
cement in the curettage bed of the distal radius with an enlarging adjacent area of
lucency (arrow). B, Coronal T1 FS Gd MRI confirms an enhancing soft-tissue mass
(arrow) consistent with recurrent tumor.
•
FIGURE 11.20 Recurrent parosteal osteosarcoma. A, Anteroposterior radiograph
shows a small destructive lesion with faint soft-tissue mineralization (arrow) at the site
of previous tumor resection and massive allograft reconstruction. B, Fused axial FDG
PET/CT image shows high glycolytic activity in the lesion (arrow). The image is
degraded by beam-hardening artifact from the metal plate.
•
FIGURE 11.21 Metastatic osteosarcoma. CT shows a lesion in the right middle lobe
with cannonball morphology and mineralization.
FIGURE 11.22 • Metastatic osteosarcoma. CT shows mineralized lesion with
sunburst morphology in the prespinal soft tissues.
•
FIGURE 11.23 Humeral head pseudolesion in a 61-year-old man with shoulder
pain. A, The arm is internally rotated and slightly abducted, so that the inferior cortex
of the anatomic neck forms an apparent sclerotic margin (arrow) around a lucent
humeral head lesion. B, When the arm is externally rotated, the pseudolesion
disappears.
•
FIGURE 11.24 False-positive in a 58-year-old woman with laboratory evidence of
myeloma. Skeletal survey showed suspicious lucent region in the right iliac wing
(arrow). Subsequent cross-sectional imaging was negative, and the lucency was
apparently overlying bowel gas.
THE SOLITARY BONE LESION

Imaging analysis of a solitary bone lesion is a skill that every radiologist should
have. The most basic task is to decide if there is actually a lesion. Normal
anatomy in unfamiliar projections and superimposed soft-tissue structures may
sometimes simulate lesions, particularly in the humerus and pelvis (Figures
11.23–11.26). Once it has been established that there is a lesion, patient factors,
the bone involved, and the location of the lesion within the bone will generally
narrow the differential diagnosis more than the appearance of the lesion itself.
Determining the rate of growth may distinguish aggressive lesions from
nonaggressive lesions, and sometimes clues to tissue characterization can lead to
a specific diagnosis. Some lesions may present with a classic radiographic
appearance that may yield to simple pattern recognition. However, for many
cases, further imaging or biopsy may be necessary.
•
FIGURE 11.25 Almost false-negative in a 25-year-old with worsening back pain that
began after a motor vehicle accident several months earlier. A, The radiograph was
remarkable for an avulsion fracture of the left iliac crest (arrow) and very subtle
sclerosis. B, Axial T1 FS Gd MRI showed a very large mass arising from the iliac wing
that proved to be Ewing sarcoma.
•
FIGURE 11.26 Humeral shaft pseudolesion in a 52-year-old woman with left
shoulder pain and history of treated breast cancer. A, Shoulder radiographs were
obtained and a lytic lesion in the humeral midshaft (arrow) was identified on the
anteroposterior radiograph. B, On the oblique radiograph, the lesion disappears.
Superimposition of soft-tissue shadows in this postmastectomy patient was
responsible for the humeral shaft pseudolesion.
References
1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2017. CA Cancer J Clin. 2017;67(1):7–30.
doi:10.3322/caac.21387 [Epub January 5, 2017. PMID:28055103].
2. Hudson TM. Radiologic-Pathologic Correlation of Musculoskeletal Lesions. Baltimore: Williams &
Wilkins; 1987.
3. Moser RP, Madewell JE. An approach to primary bone tumors. Radiol Clin North Am. 1987;25:1049–
1093.
4. Miller TT. Bone tumors and tumorlike conditions: analysis with conventional radiography. Radiology.
2008;246(3):662–674.
5. Unni KK, Inwards CY. Dahlin’s Bone Tumors: General Aspects and Data on 10,165 Cases. 6th ed.
Philadelphia: Lippincott Williams & Wilkins; 2010.
6. Fechner RE, Mills SE. Tumors of the Bones and Joints. Washington, DC: Armed Forces Institute of
Pathology; 1993.
7. Fletcher CDM, Bridge JA, Hogendoorn PCW, Mertens F. WHO Classification of Tumours of Soft Tissue
and Bone. Lyon: International Agency for Research on Cancer; 2013.
8. Lodwick GS, Wilson AJ, Farrell C, et al. Determining growth rates of focal lesions of bone from
radiographs. Radiology. 1980;134:577–583.
9. Lodwick GS, Wilson AJ, Farrell C, et al. Estimating rate of growth in bone lesions: observer
performance and error. Radiology. 1980;134:585–590.
10. Stacy GS, Mahal RS, Peabody TD. Staging of bone tumors: a review with illustrative examples. AJR
Am J Roentgenol. 2006;186(4):967–976 [PMID: 16554565].
11. Temple HT, Bashore CJ. Staging of bone neoplasms: an orthopedic oncologist’s perspective. Semin
12. Enneking WF. A system of staging musculoskeletal neoplasms. Clin Orthop Relat Res. 1986;(204):9–24
[PMID:3456859].
13. Amin MB, Edge S, Greene F, et al, eds. AJCC Cancer Staging Manual. 8th ed. New York: Springer;
2017:471–486.
1. Which radiographic feature is most characteristic of a nonaggressive bone

tumor?
A. Sclerotic margin
B. Matrix mineralization
C. Cortical penetration
D. Periosteal reaction
2. Which type of periosteal reaction is most characteristic of an aggressive bone

tumor?
A. Solid
B. Polyostotic
C. Circumferential
D. Interrupted
3. Which of the following primary bone sarcomas is the most common in adults
above the age of 40 years?
A. Ewing sarcoma
B. Chondrosarcoma
C. Chordoma
D. Fibrosarcoma
4. Which of the following primary bone sarcomas is the most common in adults
below the age of 30 years?
A. Ewing sarcoma
B. Chondrosarcoma
C. Osteosarcoma
D. Fibrosarcoma

1. A A thin, sclerotic margin indicates a nonaggressive bone lesion.
2. D Interrupted periosteal reaction indicates a high growth rate.
3. B Chondrosarcoma is the most common primary bone sarcoma above the
age of 40 years.
4. C Osteosarcoma is the most common primary bone sarcoma between the
ages of 10 and 30 years.
12
Imaging of Benign Bone Lesions
Kimia Khalatbari Kani and Felix S. Chew
Benign bone lesions are encountered during everyday radiologic practice. Many
common benign bone lesions have distinctive appearances on imaging that may
be confidently diagnosed.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of benign bone lesions, the learner
will be able to
4. summarize relevant concepts and knowledge for the following topics: bone island, osteoid
osteoma, osteoblastoma, osteochondroma, osteochondromatous lesions, chondroma,
enchondroma, enchondroma versus low-grade chondrosarcoma, periosteal chondroma,
chondroblastoma, chondromyxoid fibroma, fibrous cortical defect (FCD) and nonossifying
fibroma, fibrous dysplasia, desmoplastic fibroma, intraosseous lipoma, aneurysmal bone cyst,
simple bone cyst, intraosseous ganglion, epidermoid inclusion cyst, hemangioma, giant cell
tumor, and Langerhans cell histiocytosis (LCH).
BONE ISLAND
Bone island (enostosis) is a common incidental lesion, representing an
intramedullary hamartomatous focus of cortical bone. These lesions tend to
occur in older patients with no gender predilection.1 Bone islands are typically
painless, but giant bone islands (larger than 2 cm) may be painful.2 Bone islands
may occur in any bone and may be solitary or multiple.3 Multiple bone islands
may also occur in the context of osteopoikilosis.4 Although typically stable, bone
islands may increase or decrease in size.5
The typical appearance of bone islands on radiographs and CT is a
homogenously dense, longitudinally oriented, round or oval intramedullary
lesion (Figure 12.1).3 The lesion demonstrates radiating spicules that blend with
the surrounding trabeculae (Figure 12.2).1 On MRI, bone islands demonstrate
low T1 and T2 signal. Bone islands usually do not demonstrate increased uptake
on bone scans. Thus, bone scans may be used for the differentiation of bone
islands from other types of sclerotic bone lesions, especially osteoblastic
metastases. However, there have been reports of bone islands (especially, giant
bone islands) demonstrating increased uptake on bone scans.6 Follow-up and/or
biopsy may be indicated in presumed bone islands and in the following cases:
large lesions, lesions that are increasing in size (>25% increase in size in
6 months), lesions that demonstrate increased scintigraphic activity, symptomatic
patients, or patients with history of malignancy.6,7
OSTEOID OSTEOMA
Osteoid osteoma accounts for 11% of benign bone tumors.8 The tumor is more
commonly seen in males between 7 and 25 years of age.9 The classic
presentation is nocturnal pain that is relieved by nonsteroidal anti-inflammatory
drugs (NSAIDs). In the spine, osteoid osteomas may cause painful scoliosis of
rapid onset and neurologic deficits.8
The tumor, called the nidus, is composed of bone at various stages of maturity
in a highly vascular connective tissue stroma.10 The center of the nidus
demonstrates variable amounts of mineralization. Peripherally, variable amounts
of reactive changes (reactive bone sclerosis, cortical thickening, periosteal
reaction, bone marrow and soft-tissue edema, joint effusion, and synovitis) are
seen near the nidus.8,10 Osteoid osteoma can be seen in any bone in the
appendicular skeleton and in the spine (most commonly the posterior elements).
Involvement of the facial skeleton and skull is very rare.8 More than half of the
osteoid osteomas occur in the femur and tibia. The nidus may have a cortical
(most common), cancellous, or subperiosteal distribution.11 The lesions are
usually solitary and diaphyseal in locations. Rarely, osteoid osteomas may
involute spontaneously.
Intracortical osteoid osteomas involving the shafts of long bones usually
demonstrate a classic clinical presentation. Osteoid osteomas demonstrating
radiologic and clinical features other than the classic presentation are considered
atypical osteoid osteomas. A high index of suspicion is necessary for the
diagnosis of such atypical cases.8
•
FIGURE 12.1 Bone island. Anteroposterior left knee radiograph of a 53-year-old
man shows an oval, longitudinally oriented, giant bone island (the lesion measured
30 mm in the long axis), eccentrically located in the medullary canal of the distal
femoral diaphysis. The bone island demonstrates distinctive thorny spicules along its
periphery that blend with the surrounding osseous trabeculations.
The typical radiographic appearance of osteoid osteoma is a well-defined

round or oval intracortical nidus within the diaphysis of a long bone. The
radiolucent nidus measures less than 15 to 20 mm and demonstrates variable
central mineralization.8 Fusiform cortical thickening, reactive sclerosis, and
periosteal reaction may be evident in varying degrees near the nidus (most
commonly seen in intracortical lesions and less conspicuous or absent with
medullary and subperiosteal lesions).10 Bone density may also be decreased
secondary to pain-related disuse.10
•
FIGURE 12.2 Bone island. A, Bone island in the cancellous bone of the coronoid
process of elbow (arrow) on sagittal reformatted CT. The margin of the lesion is
spiculated and the lesion is as dense as the cortex. Olecranon spur (arrowhead). B,
Sagittal T2 FS MRI shows the bone island to have low signal intensity (arrow).
Osteoid osteomas have intensely increased activity on bone scans. In the

appendicular skeleton, osteoid osteomas demonstrate a specific appearance with
a central focus of very high radiotracer uptake and a larger surrounding area of
mildly increased uptake (double density sign or headlights in the fog).12 SPECT
may be useful in the evaluation of osteoid osteomas, especially in the spine.13
On 18F-FDG PET, the nidus demonstrates uptake, whereas the surrounding
reactive sclerosis does not.14 PET may be of value for the initial diagnosis and
posttreatment evaluation of osteoid osteomas.14
CT is the modality of choice for detection of osteoid osteomas (Figure 12.3),
especially in areas where radiographic evaluation is difficult because of complex
anatomy. MRI performed with techniques to increase spatial resolution and
contrast enhancement may be as effective as or more effective than CT for
detecting medullary osteoid osteomas.15 On MRI, the nidus demonstrates low to
intermediate T1 signal and variable T2 signal (depending on the amount of
mineralization present in the center of the nidus) (Figure 12.4). When present,
reactive bone marrow edema, soft-tissue edema, joint effusion, and synovitis are
also well evaluated on MRI.
Intra-articular osteoid osteomas occur in the joint capsule (most commonly
the hip) and usually present with nonspecific arthritic findings. Nocturnal pain
that is alleviated by NSAIDs is typically absent in such patients. When occurring
near a nonfused growth plate, these lesions have the potential to cause growth
disturbances (such as leg length discrepancy and malalignment). Imaging
findings are also atypical: reactive sclerosis is minimal to absent, whereas
regional periarticular osteopenia is typically seen early in the disease.8,10 The
nidus is best evaluated with CT, whereas MRI better depicts the associated joint
effusion and synovitis. Bone scan shows generalized increased joint uptake,
without the classic “double-density” sign.8
•
FIGURE 12.3 Osteoid osteoma in a 16-year-old adolescent boy with nocturnal left
leg pain alleviated with nonsteroidal anti-inflammatory drugs. Axial (A) and sagittal (B)
CT scans of the leg show a lucent intracortical nidus (arrows) with central
mineralization in the tibial shaft. There is adjacent fusiform cortical thickening and
subendosteal sclerosis.
Initially patients with osteoid osteomas are managed medically.16 Persistent

symptoms may necessitate further treatment with either removal or ablation of
the nidus. Currently, these lesions are mostly managed with percutaneous
techniques, with radiofrequency (RF) ablation being the most widely used
technique. Using RF ablation, excellent long-term symptom relief and success
rates have been reported.16 Failure to remove or destroy the nidus entirely may
result in recurrence.
After RF ablation, CT, MRI, or PET imaging may be used for evaluation of
the treated lesion. On CT, partial to complete replacement of the nidus with
sclerotic bone may be seen within 2 months to 2 years after ablation.16
Successfully ablated lesions may demonstrate a characteristic evolving
appearance on MRI.17 From 1 week to 2 months after ablation, the ablation zone
manifests low T1 and T2 signal with an enhancing high T2 signal rim. After
2 months, there is progressive size diminution and centripetal enhancement (with
near-complete enhancement) of the ablation zone. The ablation zone along with
the surrounding bone marrow edema involutes and resolves over the course of
several months. Persistent lucency at the ablated site on CT or increasing arterial
enhancement or bone marrow edema on MRI is concerning for residual or
recurrent tumor.16
OSTEOBLASTOMA
Osteoblastomas are uncommon, slow-growing, osteoid-forming neoplasms that
are considered by some to be giant osteoid osteomas.18 These tumors occur more
commonly in males with a mean age of 20 years.19,20 The typical presentation is
dull aching pain of several months’ duration. In comparison with osteoid
osteomas, the pain is usually less intense, is not typically nocturnal, and does not
usually respond to NSAIDs.1 Superficial lesions may present with swelling and
tenderness. Spinal lesions may present with painful scoliosis or neurological
deficits, depending on location.
Approximately a third of osteoblastomas occur in the spine, 25% to 30% arise
in the long tubular bones (most commonly the femur and tibia), and 12% to 25%
arise in the short tubular bones of the hands and feet.1 In the spine, the posterior
elements are most commonly involved. In the long bones, the lesions most
commonly occur in the medullary space or cortex (and rarely subperiosteum) of
the diaphysis or metaphysis.19,21 Osteoblastomas are benign lesions. Rarely,
osteoblastomas may be locally aggressive.20 Osteoblastomas may demonstrate
secondary aneurysmal bone cyst (ABC) formation.
•
FIGURE 12.4 Osteoid osteoma. A, Coronal T1 MRI shows subchondral lesion
(arrow) in the lateral tibial plateau. B, Coronal T2 FS MRI shows nidus (arrow) with
surrounding edema. C, Axial CT shows central ossification within the nidus (arrow).
•
FIGURE 12.5 Osteoblastoma in a 25-year-old man with a left chest wall mass. Axial
CT shows a lobulated, mixed lytic-sclerotic expansile mass with a sclerotic border
arising from the posterior aspect of the left fifth rib.
The typical radiographic appearance of osteoblastoma is a well-defined

geographic lesion that is larger than 1.5 to 2 cm, with variable osteoid matrix
mineralization (the lesions may be completely lucent or demonstrate varying
degrees of ground-glass or densely solid mineralization).1 Most lesions have a
sclerotic border.19 Cortical expansion is seen in >60% of spinal and long-bone
osteoblastomas.19 Cortical destruction is seen in 25% of long-bone
osteoblastomas and 60% of spinal osteoblastomas.19 A nonaggressive, solid or
lamellated periosteal reaction is present in approximately half of the lesions.19 In
comparison with typical osteoid osteomas, there is usually much less reactive
bone adjacent to an osteoblastoma. On bone scans, osteoblastomas typically
demonstrate nonspecific, intense radionuclide accumulation.1
Lesions can be further characterized and delineated with CT and MRI (Figure
12.5). On MRI, osteoblastomas demonstrate low to intermediate signal intensity
on T1 and variable signal intensity on T2 with variable enhancement.1 There
may be extensive bone marrow and soft-tissue edema adjacent to the lesion
(flare phenomenon), which may overestimate the lesion size on MRI.22
Treatment is usually surgical. The recurrence rate for primary curettage or
resection of osteoblastomas ranges from 8% to 19%.19,20 More recently these
lesions have been targeted with CT-guided RF ablation with excellent results.23
OSTEOCHONDROMA
Osteochondroma (exostosis) is a common lesion comprising 20% to 50% of all
benign bone tumors.24 Lesions may be solitary or multiple. Solitary
osteochondromas occur in 1% to 2% of the population and demonstrate a male
predilection.25 The vast majority of lesions are asymptomatic. Symptomatic
lesions usually present in younger (<20 y) individuals, usually as a slowly
enlarging painless lump.25 Multiple osteochondromas may be seen in hereditary
multiple exostoses (diaphyseal aclasis or osteochondromatosis) (Figure 12.6) or
in dysplasia epiphysealis hemimelica (a nonhereditary skeletal developmental
disorder characterized by single or multiple epiphyseal osteochondromas).24
FIGURE 12.6 • Osteochondromatosis (multiple hereditary exostoses).
Anteroposterior right knee radiograph of a 23-year-old man shows multiple
osteochondromas. The continuity of the cortex and medullary bone of the exostoses
with those of the parent bone is evident for the larger lesions. The exostoses point
away from the joint space.
Solitary osteochondromas are associated with mutations in the gene encoding

exostosin 1, supporting the theory that they are true neoplasms rather than a
developmental anomaly (there has also been a few case reports of
osteochondromas arising at sites of physeal injury).26 It is postulated that these
mutations ultimately result in a loss of polar organization of growth plate
chondrocytes. These chondrocytes grow in the wrong direction and
progressively undergo endochondral ossification, resulting in a bony outgrowth
that is covered by a variably thick hyaline cartilaginous cap. The thickness of the
cartilage cap is typically 1 to 3 cm in young patients, whereas in adults it is often
only a few millimeters thick or entirely absent.24 The bony outgrowth is
composed of cortical and medullary bone, which is continuous with the cortex
and medullary canal of the underlying parent bone (Figures 12.7 and 12.8).
Although any bone with enchondral ossification may be involved, lesions in the
femur, tibia, and humerus account for two-thirds of cases.27 Osteochondromas
usually arise from the metaphyses and may be sessile or pedunculated.
Osteochondromas should not enlarge after skeletal maturity. Complications of
osteochondromas include cosmetic and osseous deformity, mechanical
impingement, adventitial bursa formation, and fracture. Malignant
transformation to low-grade chondrosarcoma is very rare and occurs
predominately within the cartilage cap.24 Findings suggesting malignant
transformation include onset of pain or growth in an adult, cartilage cap
thickness greater than 2 cm in adults (Figure 12.9), irregular or indistinct lesion
margins, focal lucencies within the lesion, erosion or destruction of the adjacent
bone, and soft-tissue mass.24,28
•
FIGURE 12.7 Sessile osteochondroma in a 19-year-old man. A, Coronal T1 FS
shows bony mass extending from the medial aspect of the proximal femur, with
contiguity of the cortex and marrow space with the underlying bone. B, Coronal T2 FS
MRI shows that the cartilage cap is only a few millimeters thick (arrow).
•
FIGURE 12.8 Osteochondroma in a 35-year-old man. A and B, Axial CT with soft-
tissue and bone settings demonstrates the contiguity of cortex and marrow space of a
pedunculated osteochondroma of the proximal tibia. There is no cartilage cap.
On radiographs, osteochondromas (especially pedunculated lesions of the

long bones) demonstrate a pathognomonic appearance: a bony outgrowth
composed of cortical and medullary bone, which is continuous with the cortex
and medullary canal of the parent bone.29 However, this distinctive continuity
may not be apparent on radiographs, especially when the lesions are sessile or
arise from flat bones or the spine and may necessitate further imaging. Both CT
and MRI permit lesion characterization and assessment of cartilage cap
thickness. On CT, the cartilage cap may be nonmineralized (the attenuation of
nonmineralized cartilage is lower than that of muscle secondary to its high-water
content) or may demonstrate variable amounts of mineralization. On MRI, the
mineralized portion of the cartilage cap demonstrates low signal intensity on all
pulse sequences. The nonmineralized portion of the cap has intermediate to low
T1 signal and markedly high T2 signal.30 The cartilage cap is surrounded by a
thin hypointense line (the perichondrium) and frequently demonstrates internal
septations. After gadolinium administration, the cartilage cap demonstrates
peripheral and septal enhancement.30,31 Uptake on bone scans depends on
endochondral bone formation; lesions in adults show minimal if any uptake.32,33
OSTEOCHONDROMATOUS LESIONS
Subungual exostosis, turret exostosis, and bizarre parosteal osteochondromatous
proliferation (also called BPOP and Nora lesion) are benign bone lesions that
may resemble osteochondromas. These lesions predominately occur in the
tubular bones of the hands and feet and are likely posttraumatic in nature.
Typically, a bony mass arises from the cortex. Unlike osteochondromas, there is
no medullary continuity between the lesion and the underlying bone.24
Subungual exostosis is a common lesion arising from the dorsal or dorsomedial
aspect of the distal phalanx, with a variable relationship to the nail bed (the great
toe is most commonly affected).24 A history of trauma is elicited in up to 25% of
cases.34 Turret exostosis is a rare bony excrescence originally described as
arising from the dorsum of a proximal or middle phalanx of the hand.35 The
lesion is postulated to arise from a deep laceration to the digital extensor
mechanism of the finger, with development and subsequent maturation of a
subperiosteal hematoma.24 BPOP is a form of heterotopic ossification that most
commonly affects the metacarpals and metatarsals (76% of cases) (Figure 12.10)
and less commonly the long bones and the skull.36,37 BPOP is nonneoplastic and
thought to be reactive and possibly posttraumatic. Symptomatic lesions are
locally excised, but recurrence rates may be as high as 53%.24
•
FIGURE 12.9 Osteochondroma with a thick cartilage cap in a 39-year-old man with
a palpable left knee mass. Anteroposterior left knee radiograph shows a
superomedially protruding osteochondroma with a thick cartilage cap (29 mm) arising
from the distal femoral metaphysis. The lesion was excised (pathology was negative
for malignant degeneration).
ENCHONDROMA
Chondromas are benign neoplasms composed of mature hyaline cartilage.
Within the bones, chondromas usually occur in the medullary canal
(enchondromas) but may rarely arise juxtacortically (periosteal chondromas).
Chondromas may also arise in the soft tissues. Enchondroma is a common
benign neoplasm that is usually detected incidentally. Most patients are between
10 and 50 years of age.27 Approximately 40% to 65% of enchondromas are
found in the short tubular bones of the hand (most commonly in the proximal
phalanges).28 Pathologic fracture is a well-known presentation of hand lesions.38
Approximately 25% of enchondromas involve the long bones (most commonly
the femur, humerus, and tibia), while approximately 7% involve the feet.38
Enchondromas are typically located in the medullary canal of the metaphysis or
diaphysis of long bones. Epiphyseal lesions are uncommon.39 Multiple
enchondromatosis (Ollier disease) (Figure 12.11) is a nonhereditary diffuse
growth abnormality associated with multiple enchondromas. When there are
associated soft-tissue hemangiomas, the condition is known as Maffucci
syndrome. Solitary enchondroma rarely undergoes malignant transformation to
chondrosarcoma, but patients with multiple enchondromatosis have a 30% to
50% risk of developing chondrosarcoma.27
On radiographs and CT, enchondromas are lucent intramedullary lesions with
a lobular contour. In the hand, the lesion is typically centered in the diaphysis,
whereas in the other long bones the lesion may be diaphyseal or metaphyseal
(Figures 12.12 and 12.13).29,38 Enchondromas may be associated with variable
degrees of endosteal scalloping, cortical thinning, and osseous expansion in the
hand (these changes are usually minimal in the femur, humerus, and tibia).28
Cortical breakthrough and periosteal reaction are absent, unless a pathologic
fracture has occurred. Lesions usually demonstrate chondroid matrix
mineralization. On MRI, enchondromas demonstrate intermediate to low T1
signal and a T2 hyperintense lobular configuration characteristic for chondroid
matrix. Matrix calcifications are seen as low-signal foci on all pulse
sequences.29,38 The lobular configuration of the lesion is secondary to the
presence of thin hypointense fibrovascular septa that enhance on postcontrast
images. Lesions demonstrate mild to moderate uptake (usually less than or equal
to the anterior iliac crest) on bone scans.38 Increased activity of enchondromas
has been reported on 18F-FDG PET studies.40
How to differentiate enchondroma from low-grade chondrosarcoma? Pain
arising from the tumor is suggestive of chondrosarcoma. In the long bones of the
appendicular skeleton (excluding the tubular bones of the hands and feet), the
following imaging features are concerning for chondrosarcoma: spontaneous
pathologic fracture, permeated or moth-eaten appearance, deep and extensive
endosteal scalloping, medullary expansion, cortical destruction or penetration,
cortical thickening, periosteal reaction, soft-tissue mass, surrounding edema,
destruction of chondroid matrix over time, marked uptake on bone scan, and
early, exponential enhancement on dynamic contrast-enhanced MRI. In the
presence of suspicious findings, tumor biopsy or excision may be
indicated.27,38,41,42
PERIOSTEAL CHONDROMA
Periosteal chondroma is a rare neoplasm arising from the surface of the cortex,
deep to the periosteum. Presentation is usually in the third or fourth decades of
life as a painful swelling arising from the metaphysis of a long bone (most
commonly the humerus).28 On radiographs, the lesion is typically seen as a
lucent juxtacortical lesion with a thin periosteal shell and cortical scalloping
(Figure 12.14). Chondroid matrix calcification and smoothly contoured solid
periosteal reaction may be present.27,28 On MRI, lesions typically demonstrate a
lobular morphology with high T2 signal.
CHONDROBLASTOMA
Chondroblastoma (Codman tumor) is a rare benign bone tumor of chondroblast
origin. Most patients are between 5 and 25 years of age, and there is a male
predilection.27 Pain is the most common presenting symptom.43 Rarely
chondroblastomas may be locally aggressive or metastasize.44,45 Approximately
75% to 80% of chondroblastomas occur in the long bones (most commonly near
the knee), and more than 90% of long-bone cases involve an epiphysis or
apophysis.46 Metaphyseal extension of the lesion is commonly encountered after
closure of the growth plate. The tarsal bones (especially the talus) are the next
most common sites of involvement.46,47 On radiographs, chondroblastoma is
typically seen as an epiphyseal (metaphyseal extension may be present)
geographic lucent lesion with a thin sclerotic border and a lobulated contour
(Figure 12.15). Matrix calcification and a thick, solid periosteal reaction
occurring in the metaphysis adjacent to the epiphyseal lesion may be seen in
30% and 60% of cases, respectively.48,49 Secondary ABC develops in 15% of
cases.48 These hyperemic tumors typically show avid uptake on bone scans.50
On MRI, the tumor typically demonstrates intermediate T1 signal and is usually
T2 hyperintense (either partially or completely).51,52 Enhancement (typically
either lobular or peripheral/septal) is visualized after gadolinium administration.
Reactive, inflammatory changes are commonly seen adjacent to the tumor and
include bone marrow edema (usually marked), periostitis, soft-tissue edema,
joint effusion, and synovitis.53 Chondroblastomas are usually treated with
curettage.28 CT-guided RF ablation has also been described.54,55
•
FIGURE 12.10 Bizarre parosteal osteochondromatous proliferation. A, Radiograph
of hand shows mineralized parosteal mass (arrow) at the second metacarpal. B, Axial
CT shows the absence of contiguous marrow space between the lesion (arrows) and
underlying bone.
FIGURE 12.11 • Multiple enchondromatosis (Ollier disease). Posteroanterior
radiograph of the right hand in a 42-year-old man shows enchondromas in the second
and third digits and the distal portion of the second metacarpal bone.
•
FIGURE 12.12 Enchondroma. Oblique radiograph of the right forearm in a 35-year-
old woman. There is a lobulated geographic lytic lesion with a thin sclerotic border in
the medullary canal of the ulnar diaphysis. There are punctate matrix calcifications.
There are associated endosteal scalloping and cortical thinning with a superimposed
pathologic fracture.
•
FIGURE 12.13 Enchondroma in a 71-year-old woman presented for follow-up of
known proximal humeral lesion. A, Anteroposterior radiograph of the right shoulder
shows intramedullary chondroid calcifications in the proximal humeral metadiaphysis.
B, Coronal T2 FS MRI shows a hyperintense lesion with a distinctive lobular
configuration.
•
FIGURE 12.14 Periosteal chondroma in a 23-year-old man with a right shoulder
mass. Axial CT of the right shoulder shows a lucent juxtacortical lesion (arrow).
CHONDROMYXOID FIBROMA
Chondromyxoid fibroma is a very rare lesion composed of variable amounts of
chondroid, fibrous and myxoid elements.56 Patients usually present with pain.
The mean age at presentation is 25.1 years (range of 3-70 years).28 Most
chondromyxoid fibromas (approximately 65%) arise in the medullary canal of
the long bones of the lower extremity (most commonly around the knee).28
Lesions are usually either metaphyseal or less commonly diaphyseal in
location.57,58 On radiographs, chondromyxoid fibroma typically appears as a
metaphyseal, round, oval, or lobulated, expansile, geographic lucent lesion with
a thin sclerotic rim (Figure 12.16). Cortical destruction may be present, while
matrix mineralization occurs rarely.28 Internal trabeculations may be seen in
two-thirds of cases.28 Treatment is curettage and bone grafting.
FIBROUS CORTICAL DEFECT AND NONOSSIFYING
FIBROMA
FCD and nonossifying fibroma (NOF, fibroxanthoma) are common
nonneoplastic reactive or developmental bone abnormalities. These lesions may
be present in up to one-third of children.27 Controversy exists regarding the
terminology and etiology of these two conditions.59 FCD and NOF demonstrate
identical histologic features and have been separated based on their size,
location, and natural history. FCDs are small (generally less than 3 cm)
metaphyseal cortical defects that usually disappear spontaneously. NOFs are
typically larger (ranging in size from 1 to 7 cm) subendosteal, intramedullary
metaphyseal, or diametaphyseal lesions that typically regress spontaneously.
However, some lesions may persist over time and demonstrate interval growth
into adulthood.27,59 Lesions are usually incidental. Larger NOFs may be painful
or complicated by pathologic fracture.
FCD typically occurs in the developing skeleton (usually between 4 and
15 years of age) with a slight male predilection.27,59 FCDs are most commonly
seen along the posteromedial aspect of the distal femur, presumably as a stress-
related response at sites of tendinous attachments. Similar lesions may be seen in
the humerus at the insertion sites of the pectoralis major and deltoid muscles.
FCDs typically regress within 2 years of discovery, although some lesions may
persist into adulthood.27,59 NOF typically occurs in the developing skeleton (age
range 3-42 years) with a slight male predilection.59 Lesions usually occur about
the knee (especially the posteromedial surface of the distal femur) or the distal
tibia. Multiple NOFs may occur, sometimes in the context of neurofibromatosis
type I or Jaffe-Campanacci syndrome (a multisystemic disorder associated with
multiple NOFs and café au lait spots).59
•
FIGURE 12.15 Chondroblastoma in a 24-year-old man with left hip pain. A,
Anteroposterior radiograph of the pelvis shows a mildly expansile geographic lytic
lesion with a thin sclerotic border in the subchondral portion of the left femoral head.
B, On the coronal T1 FS Gd MR image, the lesion demonstrates partial enhancement.
•
FIGURE 12.16 Chondromyxoid fibroma in an 18-year-old man with right great toe
pain. Anteroposterior radiograph of the right great toe shows an expansile geographic
lytic lesion in the first distal phalanx with an imperceptible cortical shell medially.
FCD and NOF often have pathognomonic radiographic appearances. FCD

appears as a small lucent cortical lesion that eventually heals and becomes
sclerotic. Typically, there is no increased uptake on bone scans. NOFs
demonstrate an evolving, albeit usually diagnostic, appearance on radiographs.
The lesion progresses at a variable rate, from an eccentric, intramedullary, oval
lucent metaphyseal lesion near the physis to a scalloped lucent lesion with a thin
sclerotic rim (Figure 12.17) that may be located further away from the physis
and eventually to a sclerotic lesion that may ultimately disappear.60,61 Larger
lesions may demonstrate a trabeculated and expansile appearance.59 Minimal to
mild increased uptake may be noted on bone scintigraphy. NOFs demonstrate
variable (and at times increased) 18F-FDG uptake on PET.62 On MRI, NOFs
may demonstrate intense contrast enhancement (Figure 12.18).59
FIBROUS DYSPLASIA
Fibrous dysplasia is a common nonhereditary benign fibro-osseous lesion.63,64 It
is postulated to be a developmental abnormality that results in the replacement of
cancellous bone by immature bone and dysplastic fibrous tissue. The lesions
may present at any age (most are detected by 30 y) and demonstrate no gender
predilection.63 Lesions may be monostotic (approximately 80% of cases) or
polyostotic.64 The polyostotic form of fibrous dysplasia may present a
monomelic, unilateral or bilateral distribution.65 Polyostotic fibrous dysplasia
may be associated with precocious puberty and café au lait spots. This
constellation of findings is called McCune-Albright syndrome and mainly occurs
in girls. Rarely, fibrous dysplasia (usually the polyostotic form) may be
associated with intramuscular myxomas (Mazabraud syndrome). Monostotic
lesions occur most commonly in the long bones, ribs, and craniofacial bones.
Involvement of the pelvis and spine is common in the polyostotic form but
seldom encountered with monostotic disease. Hand involvement is
exceptional.65 The lesions of fibrous dysplasia develop during skeletal formation
and may enlarge with skeletal growth. Monostotic lesions generally become
quiescent with skeletal maturity, whereas polyostotic lesions may continue to
enlarge and demonstrate progressive deformity.63 Monostotic lesions are usually
asymptomatic and incidental. However, fibrous dysplasia may be complicated by
pathologic fracture, secondary ABC formation, deformity, and rarely malignant
transformation.63 Patients with Mazabraud syndrome may have a higher risk of
malignant transformation.66
The radiographic appearance of fibrous dysplasia is variable. Lesions are
intramedullary (with common cortical extension), may resemble ground glass
(Figure 12.19), and may be lucent, sclerotic, or of mixed opacity. Lesions are
typically well defined and may demonstrate a sclerotic rim. The lesions may be
expansile, and there may be associated endosteal scalloping and cortical thinning
or thickening. Some lesions may demonstrate a trabeculated appearance,
occasionally with calcifications.67 With cessation of skeletal growth, monostotic
lesions mature and may demonstrate increased matrix density and sclerotic rim
thickening on radiographs.63 In asymptomatic patients with characteristic
radiographic findings, further workup is usually not necessary. At initial
presentation, bone scan may be useful for demonstrating disease extent. CT may
show the sclerotic margin and the diffusely mineralized interior. On MRI, lesions
demonstrate variable signal intensity and enhancement (Figure 12.20)
(dependent on the degree of cellularity, fibrous tissue, bone trabeculae, cyst
formation, and hemorrhage within the lesion).63
•
FIGURE 12.17 Nonossifying fibroma in a 19-year-old man with nonspecific right
knee pain. A and B, Anteroposterior and lateral radiographs of the right knee show a
typical nonossifying fibroma in the distal femur. Note the lesion’s thin sclerotic rim
(arrow).
FIGURE 12.18 • Nonossifying fibroma. A, Lateral radiograph shows a mildly

expansile lesion in the posterior cortex of the proximal tibia. There is a well-defined
thin sclerotic margin. B, Axial T1 MRI shows the eccentric location of the lesion and
the sclerotic margin. C, Sagittal STIR MRI shows heterogeneous high signal within
the lesion. There is no surrounding edema.
DESMOPLASTIC FIBROMA
Desmoplastic fibroma (desmoid tumor of bone) is a rare tumor that is now
considered the osseous counterpart of soft-tissue desmoid tumors.68 Lesions may
be locally aggressive but have no malignant potential. Patients typically present
in the third or fourth decades of life, and there may be a slight male predilection.
On radiographs, the lesion may demonstrate a benign or aggressive
appearance. Typically, a lytic lesion with a narrow zone of transition is seen in
the central portion of the metaphysis or metadiaphysis of a long bone (Figure
12.21).68–70 Internal trabeculations or a sequestrum may be present, while matrix
mineralization is usually absent.68–70 Cortical breakthrough and soft-tissue mass
may be evident, especially on cross-sectional imaging. Significant T2 shortening
is usually evident on fluid-sensitive MRI sequences.68 En bloc resection is the
treatment of choice.
•
FIGURE 12.19 Monostotic fibrous dysplasia. Anteroposterior forearm radiograph
shows a geographic lesion in the medullary canal of the radial diaphysis with ground-
glass appearance.
INTRAOSSEOUS LIPOMA
Intraosseous lipomas are benign bone lesions composed of mature adipocytes.
These lesions are most commonly discovered in the fourth and fifth decades of
life and demonstrate a slight male predominance.71 Patients are usually
asymptomatic or may complain of pain. Although any bone may be involved,
lesions most commonly arise in the metadiaphyses of the long bones
(predominantly the intertrochanteric and subtrochanteric regions of the femur),
followed by the calcaneus and ileum.72 Lesions are usually intramedullary and
less likely cortical or parosteal in location.73 Although usually solitary, multiple
intraosseous lipomas (lipomatosis) may occur rarely. Malignant transformation
of intraosseous lipomas has been reported rarely.71,72
•
FIGURE 12.20 Polyostotic fibrous dysplasia. A, Anteroposterior radiograph of the
right hip in a 65-year-old man shows large lytic and sclerotic lesions in the right ilium
and right proximal femur with sclerotic margins. B, Coronal T2 FS MRI shows
heterogeneous high and low signal within the iliac and femoral lesions. C, Coronal T1
FS Gd MRI shows regions of heterogeneous enhancement. The round region of
nonenhancement in the ilium demonstrates fluid signal on the T2 weighted image. D,
Axial CT of the iliac wing preparatory to needle biopsy shows the lesion’s
nonhomogeneous density.
•
FIGURE 12.21 Desmoplastic fibroma in a 20-year-old woman with right knee pain.
Lateral radiograph of the right knee shows a geographic lytic lesion with a thin
sclerotic rim centrally located in the medullary canal of the distal femoral
metadiaphysis. The lesion is mildly expansile and demonstrates internal
trabeculations.
•
FIGURE 12.22 Intraosseous lipoma in a 57-year-old woman with left knee pain. A,
Anteroposterior left knee radiograph shows an eccentric, intramedullary, lucent lesion
with a thin sclerotic rim in the proximal tibial metaphysis. B, Axial T1 MRI shows a
hyperintense subendosteal lesion (arrow). C, Axial T1 FS MRI shows diffuse
suppression of the fat signal within the lipoma.
Intraosseous lipomas may undergo variable degrees of fat necrosis.72,74,75

Involuted lesions demonstrate varying degrees of fat, calcification, reactive bone
formation, fibrous tissue and myxomatous cystic degeneration. The imaging
appearance of lipomas is reflective of their histology.72 On radiographs, lesions
composed solely of fat typically appear as well-defined lucent lesions that may
be mildly expansile (Figure 12.22). These lesions may demonstrate a sclerotic
rim or internal trabeculations. Involuted lesions demonstrate varying degrees of
central or peripheral calcification or ossification. Lipomas usually demonstrate
absent to moderate uptake on bone scans.71 On CT and MRI, lesions composed
solely of fat demonstrate attenuation and signal intensity similar or close to the
subcutaneous fat, respectively. Lesions become progressively heterogeneous as
they involute and become partially calcified, ossified, or cystic. Nevertheless,
identification of fat in such lesions permits the definitive diagnosis of an
intraosseous lipoma.71,72 Asymptomatic or incidentally discovered lesions do not
require treatment. Symptomatic lipomas may be treated with curettage and bone
grafting.75
•
FIGURE 12.23 Aneurysmal bone cyst. A, Posteroanterior radiograph shows large
expansile second metacarpal bone lesion. B, Coronal T2 FS MRI shows loculated
fluid-filled spaces within the lesion. C, Coronal T1 FS Gd MRI shows enhancement of
the septa.
ANEURYSMAL BONE CYST

ABC is an uncommon lytic, expansile, hemorrhagic bone lesion composed of
variably sized blood-filled spaces separated by connective tissue septa with
osteoclastic giant cells and variable reactive bone. Typically, patients present in
the second decade of life with pain or swelling for less than 6 months.27 There is
a slight female preponderance. Although lesions are usually de novo (primary
ABCs), 30% of ABCs are secondary and form adjacent to a variety of benign
(most commonly giant cell tumor) or less commonly malignant tumors.76 Solid
ABC (giant cell reparative granuloma of bone) comprises <10% of ABCs.76
Surface or soft-tissue lesions may occur rarely.76,77 Primary ABC is considered
to be a neoplastic process and is associated with rearrangement and upregulation
of the USP6 oncogene (chromosome 17).76
•
FIGURE 12.24 Aneurysmal bone cyst of distal tibia. A, Axial T2 FS MRI shows
expansile intramedullary bone lesion with fluid-fluid levels (arrow). B, Coronal T2 FS
MRI shows multiple septated compartments.
The most commonly affected regions are the long bones (67% of cases; most
commonly the metaphysis), spine (15%; most commonly the posterior arch), and
pelvis (9%).76 On radiographs, ABC is typically seen as a lytic-expansile lesion
located eccentrically in the medullary canal of the metaphysis (or less commonly
diaphysis) of a long bone.76,78 The lesion may demonstrate internal
trabeculations. Lesions may have a narrow (with or without a sclerotic rim) or
wide zone of transition. Sometimes expansile lesions cause cortical interruption,
but the periosteum remains intact, albeit invisible on radiographs.27 Rarely
ABCs may extend through the growth plate and result in leg-length discrepancy
or deformity.76 In the spine, lesions may involve multiple vertebrae.
Approximately 36% of ABC cases will present with a pathologic fracture.79
Bone scan typically demonstrates increased peripheral uptake. MRI is more
helpful than CT for demonstrating the cystic nature of the lesion. On MRI, the
lesion demonstrates multiple fluid levels on fluid-sensitive sequences (Figures
12.23 and 12.24). On postcontrast MRI, enhancement of the cyst wall and septa
is typical.
Although typically benign, some ABCs demonstrate aggressive features such
as rapid growth, cortical destruction, and periosteal reaction with Codman
triangles.27,76,78 There have also been reports of spontaneous resolution. Optimal
treatment is controversial and may include curettage and packing, sclerotherapy,
embolization, radiotherapy, or medical therapy.80,81 Recurrence rates have been
reported from 0% to 50%.81
UNICAMERAL BONE CYST

Unicameral bone cyst (UBC) (also called simple bone cyst) is a common benign,
nonneoplastic cyst of uncertain etiology.82 UBC is a thin-walled, usually
unilocular cyst with serous or serosanguineous contents. Most cases occur in
patients below the age of 25 years with a male predilection.83 Lesions are
usually incidental or discovered with a pathologic fracture. The most common
location is the proximal humerus, followed by the proximal femur, calcaneus,
and ilium.84,85 The cysts arise in the metaphysis, and in children the bone will
grow away from it. Recent literature suggests that cyst activity is primarily a
function of age: Cysts occurring in children younger than 10 years are
considered active, whereas those occurring in individuals older than 10 years are
considered inactive.85 Cysts mostly disappear with skeletal maturity. Persistent
cysts rarely increase in size after closure of the growth plates.85 On radiographs,
a typical UBC is lucent, expansile (Figures 12.25 and 12.26), and centrally
located in the proximal humerus or proximal tibia.82,85 The lesion causes cortical
thinning but not penetration. Some cysts may be multilocular. If periosteal
reaction is present along the thinned cortex of the cyst wall, a pathologic fracture
is likely. A fractured fragment may drop into the cystic cavity (fallen fragment
sign; Figure 12.25) and shift with patient movement.86 On bone scan, a mild
peripheral uptake is typical.85 CT and especially MRI may be useful for
confirming the diagnosis of UBC. On CT, a homogeneous lesion with
attenuation values typical of cysts is usual. On MRI, UBCs commonly
demonstrate low to intermediate T1 signal, high T2 signal, and no more than 1 or
2 fluid levels.83 Treatment of UBCs is warranted if a pathologic fracture occurs
or is judged imminent. Different treatment options exist, with most treatment
options involving either injection of material into the cyst (eg, steroid or bone
marrow) or curettage and packing of the cyst.82,85 Treated cases are usually
followed up with radiography. Posttreatment complications include incomplete
healing of the cyst, pathologic fracture, infection, or premature closure of the
adjacent growth plate.83 On follow-up radiographs, complete opacification of the
cyst with cortical thickening is suggestive of healing. Residual or recurrent
lucency or an enlarging cyst is indicative of incompletely treated or recurrent
disease.83 Incomplete obliteration of the cyst may be of little importance if there
is good bone strength.87
•
FIGURE 12.25 Unicameral bone cyst in a 16-year-old man with acute right shoulder
pain. Anteroposterior right shoulder radiograph shows an eccentric intramedullary
lucent lesion in the proximal humeral metadiaphysis. There is a pathologic fracture
along with a dependent bone fragment (arrow) within the distal portion of this cystic
lesion.
•
FIGURE 12.26 Simple bone cyst in a 27-year-old woman with left shoulder pain. A,
Radiograph shows large lucent lesion in the proximal humerus. B, Axial T2 FS MRI
shows fluid-filled lesion occupying the medullary space of the proximal humerus. C,
Sagittal T2 FS MRI shows the lesion extending from the metaphysis into the shaft.
There is a fluid-fluid level (arrow).
INTRAOSSEOUS GANGLION
Intraosseous ganglia are nonneoplastic mucin-filled cysts of unclear etiology that
are devoid of an epithelial or synovial lining. Intraosseous ganglia are typically
located in the epiphyses. Unlike subchondral cysts, intraosseous ganglia do not
communicate with the adjacent joint space and are not associated with
osteoarthritis.88 Their peak incidence is during the fourth and fifth decades of
life. They may be incidental or symptomatic89 and occur mostly around the knee
and in the carpus. Multiple intraosseous ganglia may occur in the carpus. Large
lesions or lesions with atypical imaging features may be mistaken for a tumor.
On radiographs, intraosseous ganglion is typically seen as an oval or round
lucent lesion with a thin sclerotic rim, eccentrically located in the epiphysis or
metaphysis. Most are small (between 1 and 2 cm in maximum diameter; lesions
larger than 5 cm are rare).90 Lesions may be unilocular or multilocular. Some
lesions may be expansile or demonstrate soft-tissue extension.90 Matrix
calcification and periosteal reaction are typically absent. On bone scan,
intraosseous ganglia may demonstrate homogenously increased activity.88 On
MRI, intraosseous ganglia typically demonstrate low to intermediate T1 signal,
high T2 signal, and rim enhancement. Heterogenous enhancement of the lesion
is less common and may indicate septa. Fluid levels are uncommon. Bone
marrow edema may surround the lesion. Symptomatic lesions may be treated
with curettage and bone grafting.
EPIDERMOID INCLUSION CYST

Epidermoid cysts typically arise in the distal phalanges (fingers more than toes)
and the skull.91 It is postulated that these cysts arise from traumatic implantation
of epidermoid elements into bone. Patients are usually between 25 and 50 years
of age, and there is a male predilection.91 Lesions may be incidental findings, or
patients may present with swelling, pain, and tenderness at the affected site.92
On radiographs, these cysts typically are lucent lesions with a thin sclerotic rim.
Cortical thinning and expansion may be seen with larger lesions. Soft-tissue
swelling may be present.92
FIGURE 12.27 • Hemangioma in a 53-year-old woman with an incidentally

discovered sacral lesion on CT. A, Coronal CT shows an intramedullary lucent
geographic lesion with a thin sclerotic margin and internal trabeculations involving the
upper sacrum (negative attenuation values, compatible with fat, were detected in the
lucent portions of the lesion). B, Coronal T1 MRI shows distinctive fatty lesion with
intervening hypointense trabeculations.
VASCULAR BONE LESIONS

Benign vascular lesions of bone are usually discovered incidentally in
adults.93,94 Hemangioma is a benign proliferation of blood vessels and is very
common; lymphangioma is a benign proliferation of lymphatic channels and is
rare.95 The typical appearance of these lesions on radiographs is a focal, well-
defined, lucent lesion with irregular, coarse, thickened trabeculae (Figure 12.27).
The abnormal vascular spaces infiltrate and replace the bone, leaving irregular,
reactively thickened trabeculae. Any part of the skeleton may be affected, but
most of these lesions are found in the vertebral bodies where the thickened
trabeculae are vertically oriented and give the lesion a corduroy appearance on
radiographs. On CT, they appear as a localized region of thick, vertical
trabeculae interspersed with fat; this appearance is diagnostic. MRI shows the
presence of both fat (high T1 signal) and vascular spaces (high T2 signal with
enhancement), with interspersed low-signal trabeculae. Hemangiomas have
variable appearance on radionuclide bone and RBC scans, ranging from
photopenic to moderately increased activity.96 Hemangiomas are typically
hypometabolic on 18F-FDG PET.97 Diffuse skeletal angiomatosis, with or
without soft-tissue angiomatosis, is rare. There is no potential for malignant
degeneration, and treatment is reserved for symptomatic lesions.
GIANT CELL TUMOR

Giant cell tumor of bone (osteoclastoma) is an uncommon lesion that contains
osteoclastic multinucleated giant cells.98 Giant cells are a prominent histologic
component of the lesion, but other types of tumors may also contain giant cells.
Giant cell tumors may occur at any age in either sex, but the typical patient is a
young woman99 presenting with pain.100 Tumors are located almost invariably in
the epiphysis, with extension to the subchondral cortex and into the metaphysis.
Fewer than 2% occur adjacent to open growth plates. Giant cell tumors probably
arise in the cutback zone of the metaphysis where osteoclasts are plentiful and
active. Approximately 50% of tumors are found around the knee, but other long
bones and the sacrum are also commonly involved. Rarely, giant cell tumors
may be multicentric. The typical radiographic appearance is a geographic, lytic
tumor near the end of a long bone, extending to or very close to the subarticular
cortex (Figures 12.28 and 12.29; see also Figure 11.9). Lytic regions correspond
to nonmineralized tumor tissue, destroying and replacing cancellous bone. A
lobular pattern of growth may leave ridges or trabeculations in surrounding
bone. Giant cell tumors are often expansile and may have cystic blood-filled
regions similar to ABCs. The zone of transition from tumor to normal bone is
usually sharp and abrupt but without a sclerotic margin. Some lesions erode from
the epiphysis into the joint cavity and provoke synovitis. Approximately 10% of
patients present with pathologic fracture. Some giant cell tumors demonstrate
aggressive features, such as wide zone of transition, cortical bone penetration,
and soft-tissue mass,100 but periosteal reaction is unusual. CT or MRI may be
required to show the extent of tumor and the relationship to the adjacent joint.
On MRI, giant cell tumor demonstrates a nonspecific appearance with low to
intermediate T1 signal, variable T2 signal, and enhancement after gadolinium
administration. Giant cell tumors show uptake on radionuclide bone scan and
sometimes have a doughnut appearance, with greater activity at the margins.101
The typical treatment of giant cell tumor is curettage; adjuvant treatment of the
surgical bed with a high-speed burr, phenol, or cryotherapy; and packing with
methylmethacrylate (bone cement). The reported overall rate of recurrence may
be as high as 25%. Osteolysis at the cement-bone interface on postoperative
imaging follow-up is concerning for tumor recurrence (see Figure 11.19).98
Denosumab, a monoclonal antibody that inhibits osteoclast development, may be
used when surgery is unsuitable and may result in tumor necrosis, sclerosis, and
reconstitution of the host bone.98 There are case reports of pulmonary metastases
from giant cell tumors. Some literature suggests the existence of malignant giant
cell tumors, but these may actually represent other primary malignant lesions
where prominent giant cells were found at histology.
FIGURE 12.28 • Giant cell tumor in a 25-year-old man with left wrist pain.
Posteroanterior left wrist radiograph shows a lytic and expansile lesion that is
eccentrically located in the distal radius. The lesion extends to the subchondral
surface. Cortical destruction and soft-tissue extension are seen along the radial
aspect of the lesion.
•
FIGURE 12.29 Giant cell tumor in a 52-year-old woman with progressive knee pain.
A, Radiograph of the knee shows large lytic lesion in the proximal tibia extending to
the articular surface. There is no sclerotic margin around the lesion. There is no
periosteal reaction. B, Axial T2 FS MRI shows intermediate signal within the lesion. C,
Axial T1 FS Gd MRI shows diffuse enhancement.
LANGERHANS CELL HISTIOCYTOSIS

LCH represents a spectrum of rare disorders characterized by an abnormal
accumulation of histiocytes in various tissues. In approximately 70% of cases,
LCH is localized with disease limited to a single or a few bones and in some
cases the lungs.102 The following discussion pertains to the osseous
manifestations of localized LCH.
Although LCH lesions may be found at any age, patients usually present in
childhood or adolescence.103 Lesions may be asymptomatic and occasionally
resolve without treatment. Although any bone may be involved, lesions are most
commonly seen in the skull, followed by the mandible, ribs, pelvis, and spine.102
On imaging, the appearance of LCH ranges from benign and innocuous to
aggressive.104 The radiographic appearance of the lesions depends on the site of
involvement and the phase of the disease. In the skull, LCH typically appears as
a well-defined punched-out osteolytic lesion. The lesion may demonstrate a
characteristic beveled edge because of asymmetric destruction of the inner and
outer skull tables. A central focus of intact bone in some of the lytic lesions may
cause the appearance of a button sequestrum. A geographic appearance may
ensue when multiple lesions enlarge and coalesce. In the maxilla and mandible,
severe involvement of the alveolar ridge may produce the appearance of floating
teeth. In the ribs, lesions are typically lytic and may be expansile, whereas in the
pelvis, lesions may be lytic or lytic-sclerotic. In the spine, lesions predominately
involve the vertebral bodies, are typically lytic in the early stage, and may result
in vertebra plana. With healing, there may be partial or almost complete
restitution of the height of the involved vertebra. In the long bones, lesions are
usually seen in the diaphysis or metaphysis of the femur, humerus, and tibia.
Early lesions typically have a lytic, expansile, and aggressive appearance (Figure
12.30). Lesions may later become well defined with sclerotic margins. On bone
scans, LCH lesions demonstrate variable uptake.27 On MRI, LCH typically
demonstrates intermediate T1 signal, high T2 signal, and enhancement after
gadolinium administration. On MRI, extensive, reactive changes (low T1 and
high T2 signal) may be seen in the bone marrow, periosteum, and soft tissues
near the lesion.105 Management may be conservative or with a variety of
controversial treatment options, including curettage with or without intralesional
steroid injection.103
•
FIGURE 12.30 Langerhans cell histiocytosis in a 49-year-old woman with right hip
pain. A, Lateral radiograph of the right hip shows a geographic lytic lesion (arrow)
eccentrically located in the medullary canal of the proximal femoral diaphysis, with
posterior cortical destruction. B, Sagittal T1 FS Gd MRI shows heterogeneously
enhancing lesion (arrow) with adjacent enhancing bone marrow and soft-tissue
edema.
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4. Ellanti P, Clarke B, Gray J. Osteopoikilosis. Ir J Med Sci. 2010;179(4):615–616.
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1. Which solitary bone lesion is typically smaller than 1.5 to 2 cm in diameter at

presentation?
A. Osteoid osteoma
B. Osteoblastoma
C. Osteochondroma
D. Osteosarcoma
2. Which bone lesion may occur as a result of physical trauma?

A. Nonossifying fibroma
B. Osteochondroma
C. Chondroblastoma
D. Periosteal chondroma
3. Which bone lesion is typically located in the epiphysis or an epiphyseal
equivalent?
A. Osteoblastoma
B. Brodie abscess
C. Chondroblastoma
D. Aneurysmal bone cyst
4. Which bone lesion is typically located in the medullary space?

A. Osteochondroma
B. Nonossifying fibroma
C. Giant cell tumor
D. Osteoid osteoma

1. A Osteoid osteomas are by definition smaller than 1.5 to 2 cm, whereas
osteoblastomas are larger than 1.5 to 2 cm.
2. B Osteochondromas may result from trauma to the growing physis.
3. C Chondroblastomas are characteristically located in the epiphysis or an
epiphyseal equivalent.
4. C Giant cell tumor of bone arises in the medullary space; the other lesions
are typically or commonly located in the cortex.
13
Imaging of Malignant Bone Tumors
Felix S. Chew
This chapter describes the radiology of malignant and aggressive bone tumors.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of malignant bone tumors, the
4. summarize relevant concepts and knowledge for the following topics: osteosarcoma,
osteosarcoma variants, chondrosarcoma, chondrosarcoma variants, myeloma, Ewing sarcoma,
undifferentiated high-grade pleomorphic sarcoma of bone, chordoma, and adamantinoma.
OSTEOSARCOMA
Osteosarcomas are malignant osteoid-producing sarcomas (Table 13.1).
Although they are the most common of the primary bone sarcomas, there are
fewer than 1000 new cases per year in the United States.1,2 Eighty-five percent
of cases occur at the age of 30 years or younger, but osteosarcomas may occur at
any age. Most arise de novo, but in patients older than 40 years, as many as 15%
to 20% of osteosarcomas are associated with Paget disease, therapeutic
irradiation, or bone infarct.
Conventional (intramedullary) osteosarcoma is found within the cancellous
portion of a long or flat bone.3,4 Aggressive growth within the medullary cavity
leads to early cortical penetration and invasion of the soft tissues. The typical
longitudinal location is the metaphysis; the typical transverse location is
eccentric within the medullary cavity. An open growth plate can act as a barrier
to tumor spread, sparing the epiphysis in the immature skeleton. The common
locations are the distal femur (32% of cases), proximal tibia (15%), proximal
femur and femoral shaft (9%), proximal humerus (8%), and ilium (7%). Note
that nearly 50% of osteosarcomas occur around the knee.
The typical clinical presentation is nonspecific: pain, swelling, and limited
joint motion for a few weeks or months. Some patients present with pathologic
fractures, especially those with rapidly growing, sparsely ossified tumors. An
osteosarcoma may be overlooked in the presence of a healing pathologic
fracture, but appreciation of the presence of bone destruction leads to the correct
diagnosis. Fracture callus and osteosarcoma can be virtually indistinguishable
histologically.
Most osteosarcomas are heavily or moderately ossified, with the dense blastic
areas corresponding to mineralized osseous matrix made by the tumor and
reactive medullary bone (Figures 13.1 and 13.2). Lytic areas, when present,
correspond to destruction and replacement of bone by tumor tissue containing
scant or no ossification. Cortical penetration with a large soft-tissue mass is
common. Confluent bone densities within a soft-tissue mass correspond to a
mineralized matrix. A reactive periosteal new bone may have a linear, laminated,
or perpendicular sunburst bone configuration, all of which are indicative of
cortical penetration. Approximately 50% of osteosarcomas have features typical
enough to allow a confident radiologic diagnosis. Approximately 25% of
osteosarcomas are chondroblastic, with large amounts of chondroid matrix
mixed with the osteoid, so that the appearance on imaging may resemble a
chondroid or myxoid lesion. Approximately 25% of osteosarcomas are
fibroblastic, with large amounts of fibrous matrix. Recurrent tumors resemble
the primary. Any cloudlike, solid, dense bone formation within the medullary
cavity, even in the absence of overt bone destruction and soft-tissue extension,
should suggest the possibility of an osteosarcoma.
Osteosarcoma metastasizes to the lung, where the deposits may form dense,
mineralized osteoid, accumulate bone-scanning agents, cavitate, and cause
pneumothorax. At presentation, 10% to 20% of patients have metastases, usually
to the lungs. Occasionally, skip metastases occur in the medullary cavity of the
host bone, sparing an interval of normal marrow between the primary tumor and
the metastasis (Figure 13.3). A metastasis may even skip across a joint.
Table 13.1 MAIN TYPES of Osteosarcomas
Intramedullary (central)
Osteoblastic (conventional)
Chondroblastic
Fibroblastic
Telangiectatic
Small cell
Well-differentiated
Surface
Parosteal
Periosteal
High-grade surface
Intracortical
Extraskeletal
Based on Klein MJ, Siegal GP. Osteosarcoma: anatomic and histologic
variants. Am J Clin Pathol. 2006;125(4):555–581.
Osteosarcomas are rapidly growing tumors with a median doubling time of

34 days. Local recurrences are usually apparent within the first year. The current
treatment consists of neoadjuvant chemotherapy to reduce the tumor mass,
aggressive resection of the tumor, adjuvant chemotherapy, and resection of
pulmonary metastases.5 Segmental limb-sparing resections may improve
function without necessarily compromising local control. The disease-free,
overall 5-year survival rate of those without metastatic disease at presentation
(up to stage II-B) approaches 80%.
OSTEOSARCOMA VARIANTS
There are a number of recognized osteosarcoma variants.2–4,6,7 Radiation-
induced osteosarcomas have the radiologic appearance and biologic behavior of
conventional high-grade intramedullary osteosarcomas (Figure 13.4).
Approximately 5% of osteosarcomas are postirradiation in etiology.
Osteosarcoma is the most common type of postirradiation musculoskeletal
sarcoma.
Telangiectatic osteosarcomas represent approximately 4% of all
osteosarcomas and display distinctive pathologic features. The lesions are
destructive and lytic, with large extraosseous masses incompletely surrounded
by thin shells of bone (Figure 13.5). They grow rapidly and elicit relatively little
bone reaction. Pathologically, telangiectatic osteosarcomas are mostly cystic and
vascular, containing little or no tumor matrix or other solid tumor tissue. Fluid-
fluid levels may be demonstrated on CT or MRI. Telangiectatic osteosarcomas
were previously thought to be more lethal but were subsequently shown to have
the same prognosis as conventional osteosarcomas with neoadjuvant
chemotherapy and wide resection.
Parosteal osteosarcomas represent 6% to 9% of osteosarcomas. This variety
arises on the cortical surface and affects a slightly older age group, with most
patients older than 20 years. Virtually all are found in the metaphysis of a long
bone, especially the posterior surface of the distal femoral metaphysis (66% of
cases). The presentation is a nonspecific, often dull, aching pain or mechanical
difficulties caused by the mass itself. The lesions are commonly diagnosed and
treated incorrectly for years as atypical osteochondromas that somehow recur
locally. Even with late diagnosis, the prognosis is often better than for
conventional osteosarcoma. The radiographic appearance is a lobulated
juxtacortical mass with densely ossified tumor tissue attached to the cortex, often
by a stalk; variable amounts of lucent, nonossified tissue are usually present,
making the lesion larger than apparent on plain radiographs (Figure 13.6). CT or
MRI can document tumor invasion of the medullary cavity by direct extension
through the stalk.
Periosteal osteosarcomas are found in a periosteal location most commonly
along the shaft of the femur or tibia. These osteosarcomas are generally
chondroblastic and therefore not densely ossified (Figure 13.7). They are
predominantly radiolucent on radiographs and CT, with a lobulated morphology.
A sunburst appearance is often present. On MRI, the bulk of the lesion typically
has heterogeneous low T1 signal and high T2 signal. The age of onset is similar
to conventional osteosarcomas, and periosteal osteosarcomas are of moderate
histologic grade and biologic aggressiveness.
Other osteosarcoma variants with distinctive histologic or clinical features
account for approximately 1% of all osteosarcomas. These include multifocal
osteosarcoma (synchronous and asynchronous types), small cell osteosarcoma,
intraosseous well-differentiated osteosarcoma, intracortical osteosarcoma, and
high-grade surface osteosarcoma.
CHONDROSARCOMA
Chondrosarcomas are malignant cartilage-producing tumors that arise de novo or
in preexisting cartilage lesions or rests.2–4 They present a wide variation in form
and aggressiveness, and low-grade malignant lesions may be almost
indistinguishable morphologically from benign cartilage-containing lesions.8 A
limited focus of malignancy may be embedded in a much larger mass of clearly
benign tissue. At the other end of this spectrum are high-grade, frankly
malignant tumors that recur and spread by local extension or metastasis.
Chondrosarcomas follow a slow clinical evolution; they tend to metastasize late
in the clinical course, and patients rarely present with metastatic disease.9
Medullary (central) chondrosarcomas are primary lesions that arise within
cancellous bone or the medullary cavity. The most common locations are the
pelvis (23% of cases), femur (22%), ribs (11%), and humerus (11%). The
presenting symptom is deep pain lasting for months or years. If the tumor has
breached the cortex, local swelling may be present. Presentation is over a wide
age range, but most patients are between the ages of 35 and 70 years, and men
are affected more frequently than women. The treatment is surgical. The
incidence of metastasis and the prognosis are related to the histologic grade, with
10-year survival ranging from 28% for high-grade lesions to 85% for low-grade
lesions. The radiographic appearance is osseous destruction with matrix
mineralization characteristic of cartilage. A typical lesion would be a lucent area
in the center of a long bone with endosteal scalloping, cortical thickening, and
geographic margins. Often, the tumor contains the punctate or flocculent
calcification and ring-shaped ossification characteristic of cartilage tissue
(Figures 13.8–13.10). The lucent appearance is a result of the replacement of
normal bone by noncalcified cartilage. On CT, the nonmineralized regions have
a myxoid appearance with attenuation in the range of 10 to 30 Hounsfield units
(HU). On MRI, these regions have high T2 signal and variable T1 signal. A
lobular growth pattern is often evident on CT or MRI. The bone scan shows
increased tracer accumulation.
•
FIGURE 13.1 High-grade intramedullary osteosarcoma in a 24-year-old man. A and
B, Anteroposterior and lateral radiographs show large mineralized lesion in the distal
femoral metaphysis with anterior soft-tissue extension. C, Axial T1 FS Gd MRI shows
a mass occupying the entire cross section of the medullary space with diffuse
penetration through the cortex into the soft tissues. The mineralized portions of the
mass have dark signal, whereas the remainder enhances. Portions of the periosteum
show sunburst reaction. D, Sagittal T1 FS Gd MRI shows soft-tissue mass
surrounding the distal femur and involving the knee joint anteriorly.
Exostotic (peripheral) chondrosarcomas arise in the cartilage cap of a

previously benign exostosis (osteochondroma) or from the surface of a bone
involved by multiple heritable exostoses. They represent approximately 15% of
chondrosarcomas. Men are affected twice as often as women. A wide age range
is affected, but most patients are young adults. The tumors tend to be of low
histologic grade and may be difficult to distinguish from the cartilaginous cap,
but a nonmineralized soft-tissue component larger than 1 cm should raise
suspicion. If a lesion recurs, it tends to be of a higher histologic grade. The
radiographic appearance is that of an exostosis with an attached mass of soft-
tissue density containing variable amounts of cartilaginous calcification (Figure
13.11). CT and MRI reliably demonstrate a nonmineralized cartilaginous matrix.
Serial films may document destruction of ossified portions of the underlying
exostosis. These lesions appear as areas of increased tracer uptake on bone scan,
with the intensity of radionuclide accumulation roughly proportional to the
combined amount of enchondral ossification, osteoblastic activity, and
hyperemia in the tumor. The intensity of uptake does not reliably predict whether
the lesion is benign or malignant.
•
FIGURE 13.2 Osteosarcoma of the proximal tibia. A, Anteroposterior radiograph
shows a mixed lytic-blastic lesion. B, Coronal T1 FS Gd MRI shows the full extent of
the lesion.
•
FIGURE 13.3 High-grade intramedullary osteosarcoma with skip metastasis. A,
Sclerotic metastasis (arrow) is present in the proximal femur. B, Primary lesion
(arrow) is present at the distal femur.
Dedifferentiated chondrosarcomas contain a limited focus of anaplastic

sarcoma within a larger mass of typical low-grade chondrosarcoma. The clinical
course is that of the higher-grade tumor, and the prognosis is grim. These
account for approximately 11% of chondrosarcomas. Other chondrosarcoma
variants with distinctive histologic or gross pathologic features comprise
approximately 5% of all chondrosarcomas. These include clear cell
chondrosarcoma, mesenchymal chondrosarcoma, and juxtacortical (parosteal or
periosteal) chondrosarcoma.
MYELOMA
Multiple myeloma is a malignant neoplasm of plasmacytes, the cells of the bone
marrow that make immunoglobulins.10 Being the most common primary tumor
arising in bone, myeloma has an incidence in the United States of approximately
30 300 per year.11 The age of onset is usually between 45 and 80 years.
Although palliative treatments exist, the condition is uniformly fatal and without
cure.12 Myeloma arises in the bone marrow and involves it diffusely. Bony
abnormalities usually occur at multiple sites, including the vertebrae in 66% of
patients, the ribs in 45%, the skull in 40%, the shoulder girdle in 40%, the pelvis
in 30%, and the long bones in 25%. Myeloma lesions are sharply defined, purely
lytic areas of bone destruction with no reactive bone formation. The pattern of
destruction may be geographic, moth-eaten, or permeated; involvement may be
so diffuse that the bones are simply osteopenic or even normal in radiographic
appearance (Figure 13.12). Pathologically, the marrow and bone have been
replaced by myeloma tissue. Focal holes in the involved bones are filled with
closely packed sheets of plasmacytes of varying maturity. The lesions may be
expansile, penetrate the cortex, and form large extraosseous soft-tissue masses.
Pathologic fractures are common. The radionuclide bone scan is typically
normal or may show areas of decreased uptake (“cold” spots). These cold spots
represent destruction and replacement of bone by myeloma tissue without
evocation of osteoblastic bone reaction. For this reason, the plain-film skeletal
survey is the best method for disclosing sites of bone destruction. MRI shows the
replacement of the normal marrow by myeloma tissue (Figure 13.13).
•
FIGURE 13.4 Radiation-induced osteosarcoma of the scapula. A, Anteroposterior
radiograph shows radiation change in the clavicle and scapula, with coarsened
trabecular bone pattern. The humerus overlies a destructive lesion of the scapular
spine. B, Axial T2 FS MRI shows heterogeneous high signal in a large scapular mass
with soft-tissue extension (arrow).
Several differential points may help distinguish between multiple myeloma

and osseous metastases (Table 13.2) in a patient with multiple destructive bone
lesions. Myeloma tissue produces a number of osteoclast-stimulating factors that
result in bone destruction that is cleanly marginated and purely lytic. Although
metastases also produce osteoclast-stimulating factors, they tend to provoke
reactive bone, frequently resulting in a more ragged and irregular appearance.
Myeloma may involve the intervertebral discs and the mandible, but metastases
rarely do so. Metastases often involve the vertebral pedicles, but myeloma rarely
does so. A large soft-tissue mass is more likely to be present with myeloma than
with metastases. The bone scan is usually positive in the presence of bone
metastases and often negative in myeloma.
Solitary myeloma (plasmacytoma) is myeloma that has a single focus of
involvement. The findings from marrow aspiration may therefore be negative,
and laboratory manifestations may be absent. Virtually all patients with solitary
myeloma develop multiple myeloma, but 10 years or more may pass before the
progression of disease becomes apparent. Solitary myeloma commonly presents
as an expansile lesion in the spine, a rib, the pelvis, or the sacrum (Figures 13.14
and 13.15).
PRIMARY LYMPHOMA
Lymphoma presenting as a primary tumor of bone without concurrent regional
lymph node or visceral involvement represents 5% of all extranodal (non-
Hodgkin) lymphomas.13 Most are large cell lymphomas of B-cell origin and are
histologically similar or identical to extranodal lymphomas arising at other sites.
Lymphoma may develop at any age, but most patients are adults, and men are
affected more frequently than women. The common presentation is localized
pain, often with a mass, and minimal or absent systemic symptoms.
Approximately 50% have symptoms for a year or longer before diagnosis. Most
lesions have a diaphyseal location in a long bone, especially the femur or
humerus, but other frequent sites of involvement include the clavicle, ribs, and
pelvis. Ill-defined, permeated, or moth-eaten destruction of bone with little or no
periosteal reaction is the usual radiographic appearance.14 This appearance
reflects the insidious spread of tumor cells along the marrow spaces and through
the cortex by way of the haversian systems, growing through and enlarging
them. The lesions may be extensive at presentation, often involving more than
50% of the affected bone. A large, nonmineralized soft-tissue mass may be
present when there is extensive cortical destruction. Mild to moderate bone
reaction is seen in approximately 45% of lesions, consisting of a mottled
sclerotic reaction within cancellous bone, new reactive periosteal bone, or both
(Figure 13.16). Sequestra were seen in 11% of the cases of primary lymphoma of
bone. Lymphoma always shows increased isotope uptake on bone scan. CT and
MRI are useful for demonstrating tumor extent, especially cortical penetration
and extraosseous tumor. Hodgkin lymphomas may also present with
involvement of bone (Figure 13.17). The treatment of lymphoma involves
radiation therapy, adjuvant chemotherapy, and sometimes surgery. The prognosis
is related to cell type, pattern of disease, and extent of dissemination at
presentation. With optimal treatment, the 5-year survival rate is greater than
75%.
FIGURE 13.5 • Telangiectatic osteosarcoma in a 44-year-old man. A and B,

Radiographs show a lytic and sclerotic destructive lesion in the medial diametaphysis
of the left distal femur with cortical penetration and periosteal reaction (arrow). C,
Axial CT shows the eccentric involvement and 2 regions of cortical penetration. There
is layered periosteal reaction and Codman triangle (short arrow) adjacent to the
anterior cortical defect and matrix mineralization (long arrow) near the other. D and E,
Axial T1 and T2 FS MRI show the lesion has solid and cystic components, with
multiple fluid-fluid levels. The tumor extends into the soft tissues through the cortical
defects.
EWING SARCOMA FAMILY OF TUMORS

Ewing sarcoma family of tumors is a group of malignant tumors formerly called
Ewing sarcomas, primitive neuroectodermal tumors, and Askin tumors. They
have morphologically similar small round cells, a common chromosomal
translocation, and most importantly, the same biological behavior and response
to therapy.2,15,16 When primary to bone, the term Ewing sarcoma persists; when
primary to soft tissue, the term extraosseous Ewing sarcoma may be used.
Although 75% of Ewing sarcomas occur in patients younger than 20 years, these
lesions may develop at any age. They are the most common primary bone tumor
in the first decade of life and the second most common (behind osteosarcoma) in
the second decade of life.17 Patients present with local pain and swelling, fever,
anemia, and elevated erythrocyte sedimentation rate; the clinical impression is
often that of osteomyelitis. Up to 30% of patients have metastases at
presentation. Ewing sarcoma may develop in practically any bone, although the
majority of cases involve the sacrum, innominate bone, and long bones of the
lower extremities. Only 3% of tumors affect the hands and feet. Most Ewing
sarcomas are found in the metadiaphysis of long bones, mostly the femur, but
they also occur in the diaphysis and metaphysis. Approximately one-fourth
occur in flat bones (pelvis and scapula). The tumor begins in the medullary space
and spreads through the bone, often causing only minimal osseous destruction.
The tumor penetrates the cortex by extending through the haversian systems into
the subperiosteal space where the tumor may enlarge, lift the periosteum off the
bone, and eventually penetrate it to form an extraosseous mass.4 As further
destruction of the cortex occurs, a permeated pattern of bone destruction may
become evident. In the long bones, the typical radiographic appearance is that of
permeated intramedullary bone destruction with periosteal reactive bone
(Figures 13.18–13.20). Sclerotic bone reaction within the bone is usually not
seen, but on bone scan, intense radionuclide activity is present. Pathologic
fractures occur in a small number of cases. CT and MRI scanning define the
extraosseous and intramedullary components of the tumor and are useful in
planning radiation portals and in following response to radiation and
chemotherapy. A surrounding zone of edema is commonly present. Ewing
sarcoma is highly radiosensitive. Radiation and chemotherapy may be used
alone or in combination with surgical excision.18 However, the rate of local
tumor recurrence ranges from 12% to 25%. Soft-tissue extension is associated
with increased risk of distant metastases and local recurrence. Five-year survival
for nonmetastatic tumor confined to the bone of origin is 87%, but survival drops
to 20% with extraosseous extension. Patients who survive for several years may
eventually develop secondary, radiation-induced sarcomas.
•
FIGURE 13.6 Parosteal osteosarcoma. A, Lateral radiograph shows large partially
ossified mass arising from the posterior cortex of the distal femur. B, Axial CT shows
lesion arising from the surface of the posterior femoral cortex with heterogeneous
mineralization. There is no continuity of the lesion with the medullary space. C, Axial
T1 FS Gd MRI shows lack of involvement of the medullary space and heterogenous
enhancement. The popliteal neurovascular bundle has been displaced.
•
FIGURE 13.7 High-grade surface osteosarcoma in a 51-year-old man. A and B,
Anteroposterior and lateral radiographs show mineralized lesion arising from the
anterior tibial cortex. C, Axial CT shows the lesion arising from tibial cortex with fluffy
partial ossification of the soft-tissue mass. The mass does not have an organized
cortical or trabecular structure. The medullary space is uninvolved.
•
FIGURE 13.8 Central chondrosarcoma in the pelvis arising from enchondroma. A,
Radiograph shows calcified lesion (arrow) in acetabulum. B, Coronal reformatted CT
shows mildly expansile, calcified, intraosseous lesion (arrow). C, Coronal T2 FS MRI
shows high signal in the nonmineralized portions of the lesion (arrow).
•
FIGURE 13.9 Low-grade chondrosarcoma of the scapula. A, Anteroposterior
radiograph shows a well-circumscribed, mildly expansile lesion in the acromion
process (arrow) with cartilage-type calcifications. B, Axial CT demonstrates endosteal
scalloping and chondroid matrix (arrow).
FIGURE 13.10 • Low-grade chondrosarcoma of the femur. A, Anteroposterior

radiograph of the femur shows an intramedullary lesion with flocculent calcification. B,
Coronal STIR MRI shows high signal in a lobular morphology. C, Axial CT shows
endosteal scalloping (arrow) and mineralized matrix. There is no cortical penetration.
UNDIFFERENTIATED HIGH-GRADE PLEOMORPHIC

SARCOMA OF BONE
Undifferentiated high-grade pleomorphic sarcoma is a high-grade bone sarcoma
of unknown tissue lineage. The lesions that were formerly classified as
malignant fibrous histiocytoma (MFH) of bone would currently fall under this
classification, which appeared in the fourth edition of the WHO classification of
tumors of bone.2 The extant knowledge ascribed to MFH of bone generally
applies to undifferentiated high-grade pleomorphic sarcoma, a rare lesion found
in adults with nonspecific symptoms and aggressive imaging features.3
Undifferentiated high-grade pleomorphic sarcoma of bone can occur de novo,
but 10% to 20% occur in association with other osseous abnormalities such as
Paget disease and bone infarct (Figure 13.21) or after radiation therapy. The
most common sites are similar to those in osteosarcoma: the ends of long bones
(75%), with a preponderance in the lower extremity. The femur (45%), tibia
(20%), and humerus (9%) are the bones most often involved. The metaphyseal
region is the most common location within bone, and extension into the
epiphysis or diaphysis is frequent. The lesions have an aggressive appearance
with permeated or moth-eaten destruction involving a poorly defined unifocal
lesion. Cortical destruction and soft-tissue mass are almost invariably present,
and cortical expansion is unusual except in the flat and irregularly shaped bones
(such as ribs, scapula, and sternum). Periostitis is unusual unless a healing
pathologic fracture is present. Mottled internal calcifications or sclerotic margins
are rarely present. On CT, the lesions have intermediate attenuation (30 to 60
HU), with hypodense regions representing necrosis. MRI may be helpful to
assess intraosseous versus extraosseous extension. Increased uptake is seen on
bone scan. The treatment is surgical, with no clearly defined role for
chemotherapy or radiotherapy. However, the prognosis is poor because of high
rates of local recurrence and early metastases to regional lymph nodes and other
distant sites. The reported 5-year survival ranges from 0% to 70%, depending on
the stage of the lesion.
•
FIGURE 13.11 Exostotic chondrosarcoma in a patient with multiple hereditary
exostoses. A, CT scout of pelvis shows deformity of right hemipelvis from multiple
exostoses. B, Axial CT shows low-attenuation soft-tissue mass (arrow) with dense
calcifications. C, Axial T2 FS MRI shows the noncalcified areas of the mass to be of
predominately high signal (white arrow).
CHORDOMA
Chordomas are slow-growing malignant neoplasms that arise from notochordal
remnants.2,3 They are typically seen in middle-aged men, most frequently at the
ends of the spine (50% in the sacrum or coccyx, 35% in the clivus, and 15%
elsewhere in the spine). Patients present with pain of insidious onset and
symptoms caused by mass effect, often of long duration. Grossly, these tumors
are multilobular, soft, myxoid, gelatinous masses that infiltrate locally and may
eventually metastasize. In the sacrococcygeal region, the radiologic appearance
is geographic bone destruction and replacement of bone by nonmineralized
tumor.4 The margins range from sclerotic to ill-defined. The cortex is often
penetrated with the formation of a large, lobular, extraosseous mass anterior to
the spine (Figure 13.22). The tumors are typically large at presentation. Because
of the myxoid matrix, the attenuation on CT is typically lower than cellular soft
tissue, and MRI may show high T1 and T2 signal. The treatment is surgical, but
complete excision is rarely possible because of their central location. A high rate
of local recurrence and progressive difficulties in treating the recurrences result
in a poor long-term prognosis. A secondary component of high-grade sarcoma
resembling MFH (dedifferentiated chordoma) may appear after multiple
recurrences.
•
FIGURE 13.12 Multiple myeloma. Axial CT shows expansile lytic destruction of L1
vertebral body (arrows) with pathologic transverse process fracture (arrowhead).
ADAMANTINOMA
Adamantinoma is a primary low-grade malignant tumor of bone.2,3 It is of
epithelial origin, with marked predilection for the tibia. Adamantinoma is often
associated with osteofibrous dysplasia, and some authorities believe that they are
subsets of the same disease. Adamantinoma of bone is distinct from gnathic
adamantinoma (ameloblastoma), although both share an epithelial origin and a
microscopic resemblance. Although 50% present at ages 10 to 30 years,
adamantinoma may be found at any age. Symptoms of pain are often present for
more than a year, and 90% involve the tibia. A few patients have an ipsilateral
fibular tumor. The radiographic appearance is that of an eccentrically located
lucent lesion with lobulated expansion of the cortex and sharply defined margins
(Figure 13.23).4 The most common location is the tibial diaphysis with
involvement of the anterior cortex. An anterior tibial bowing deformity is
common. Approximately 90% involve the cortex and medullary space, 10% are
confined to the cortex, and 15% penetrate the cortex and involve the soft tissues.
The treatment is surgical, with a high rate of recurrence after curettage and a
lower rate after wide excision. Metastases to lung, nodes, or bone may present
many years later.
Table 13.2 DISTINGUISHING FEATURES OF MULTIPLE MYELOMA AND METASTASES
Myeloma Metastases
Margin Cleanly marginated Irregular, more ragged
Mandible Yes Rarely
Pedicle Rarely Yes
Disk space Yes Rarely
Soft-tissue mass More likely Less likely
Bone scan Negative Positive
•
FIGURE 13.13 Multiple myeloma. A, Coronal T1 MRI showing multiple lesions
(arrows) in the marrow with signal intensity similar to muscle. B, Coronal T2 FS MRI
shows corresponding high signal intensity of the lesions (arrows).
•
FIGURE 13.14 Plasmacytoma in a 52-year-old man with negative workup for
myeloma. A, Radiograph shows mildly expansile, lytic lesion involving the bicipital
tuberosity of the proximal radius (arrow). B, Coronal CT confirmed the lesion and
showed cortical thinning but no reactive bone formation. C and D, Axial T1 and T2 FS
MRI show the lesion replacing the normal marrow.
FIGURE 13.15 • Plasmacytoma. A, Axial CT with soft-tissue window shows

expansile, lytic lesion in acetabulum and superior pubic ramus. B, Axial CT with bone
window shows areas of cortical destruction.
•
FIGURE 13.16 Diffuse large B-cell lymphoma. A, Anteroposterior radiograph shows
subtle fullness of the right pelvic soft tissues. B, Axial STIR MRI shows massive
involvement of the right hemipelvis including the iliac wing, sacrum, and contiguous
soft tissues.
•
FIGURE 13.17 Hodgkin lymphoma in a 52-year-old man with knee pain. A,
Radiographs were normal. B, Coronal T1 MRI shows a lesion replacing the marrow in
the medial femoral condyle, extending into the metaphysis. C, Coronal T2 FS MRI
shows high signal in the lesion, but not as high as the joint fluid. D, Axial T1 FS Gd
MRI shows diffuse enhancement of the lesion with adjacent soft-tissue abnormality
and intact intervening cortex.
•
FIGURE 13.18 Ewing sarcoma of the distal humerus. A, Anteroposterior radiograph
shows a lytic lesion in the distal humerus at the olecranon fossa (arrow). The margins
of the lesion are irregular, and there is no reactive bone formation. B, Axial CT shows
the destructive bone lesion (arrow) with anterior and posterior soft-tissue extension.
C, Sagittal T2 FS MRI shows a mass centered at the distal humerus with large
anterior and posterior soft-tissue components (arrows). The lesion has heterogeneous
high signal. An elbow effusion is present.
•
FIGURE 13.19 Ewing sarcoma of the rib. Enhanced CT shows rib destruction and
massive soft-tissue mass (arrow).
•
FIGURE 13.20 Ewing sarcoma of the femoral shaft. A, Axial CT shows onionskin
periosteal reaction in the femoral cortex with soft-tissue density replacing normal fatty
marrow. B, Axial T2 FS MRI shows onionskin periosteal reaction and surrounding
edema.
•
FIGURE 13.21 Undifferentiated pleomorphic sarcoma of bone arising in marrow
infarct. A, Anteroposterior radiograph of the distal femur shows permeated bone
destruction (arrow). B, Axial CT shows bone destruction surrounding an irregularly
shaped sequestrum (arrow) of bone. C, Coronal T1 MRI shows the lesion (long arrow)
in the distal femur and a marrow infarct (short arrow) in the proximal tibia.
•
FIGURE 13.22 Chordoma in a 50-year-old man. A, Anteroposterior radiograph
shows destructive lesion of the lower sacrum partially obscured by bowel contents. B,
Sagittal T1 MRI shows a destructive mass arising from the S3 and S4 vertebral
bodies protruding anteriorly into the soft tissues and displacing the rectum. C, Sagittal
T1 FS Gd shows heterogeneous enhancement of the lesion.
•
FIGURE 13.23 Adamantinoma of the tibia. A, Lateral radiograph shows 2 mildly
expansile partially lucent lesions in the anterior tibial cortex with surrounding
sclerosis. B, Sagittal CT shows the lesions confined to the cortex. C, Sagittal STIR
MRI shows high and low signal within the lesions. There is overlying subcutaneous
edema. The marrow space is normal. D and E, Axial CT through the proximal and
distal lesions show remodeled cortex and trabeculae. F, Axial T2 FS MRI shows the
lesion and overlying soft-tissue edema.
References
1. Ottaviani G, Jaffe N. The epidemiology of osteosarcoma. Cancer Treat Res. 2009;152:3–13.
doi:10.1007/978-1-4419-0284-9_1 [PMID:20213383].
2. Fletcher CDM, Hogendoorn PCW, Fredrik Mertens F, Bridge J, eds. WHO Classification of Tumours of
Soft Tissue and Bone. 4th ed. Lyon: World Health Organization; 2013.
3. Fechner RE, Mills SE. Tumors of the Bones and Joints. Washington, DC: Armed Forces Institute of
Pathology; 1993.
Wilkins; 1987.
5. Ferrari S, Palmerini E. Adjuvant and neoadjuvant combination chemotherapy for osteogenic sarcoma.
Curr Opin Oncol. 2007;19(4):341–346.
6. Murphey MD, Robbin MR, McRae GA, et al. The many faces of osteosarcoma. RadioGraphics.
1997;17:1205–1231.
7. Klein MJ, Siegal GP. Osteosarcoma: anatomic and histologic variants. Am J Clin Pathol.
2006;125(4):555–581.
8. Flemming DJ, Murphey MD. Enchondroma and chondrosarcoma. Semin Musculoskelet Radiol.
2000;4(1):59–71 [PMID:11061692].
9. Riedel RF, Larrier N, Dodd L, Kirsch D, Martinez S, Brigman BE. The clinical management of
chondrosarcoma. Curr Treat Options Oncol. 2009;10(1–2):94–106. doi:10.1007/s11864-009-0088-2
[Epub Feburary 24, 2009. PMID:19238552].
10. Angtuaco EJ, Fassas AB, Walker R, Sethi R, Barlogie B. Multiple myeloma: clinical review and
diagnostic imaging. Radiology. 2004;231(1):11–23.
11. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2017. CA Cancer J Clin. 2017;67(1):7–30.
doi:10.3322/caac.21387 [Epub January 5, 2017. PMID:28055103].
12. Ludwig H, Strasser-Weippl K, Schreder M, Zojer N. Advances in the treatment of hematological
malignancies: current treatment approaches in multiple myeloma. Ann Oncol. 2007;18 (suppl 9):ix64–
ix70.
13. Durr HR, Muller PE, Hiller E, et al. Malignant lymphoma of bone. Arch Orthop Trauma Surg.
2002;122:10–16.
14. Mulligan ME, McRae GA, Murphey MD. Imaging features of primary lymphoma of bone. AJR Am J
Roentgenol. 1999;173:1691–1697.
15. Maheshwari AV, Cheng EY. Ewing sarcoma family of tumors. J Am Acad Orthop Surg. 2010;18(2):94–
107 [PMID:20118326].
16. Biswas B, Rastogi S, Khan SA, et al. Outcomes and prognostic factors for Ewing-family tumors of the
extremities. J Bone Joint Surg Am. 2014;96(10):841–849. doi:10.2106/JBJS.M.00411
[PMID:24875025].
17. Unni KK, Inwards CY. Dahlin’s Bone Tumors: General Aspects and Data on 10,165 Cases. 6th ed.
Philadelphia: Lippincott Williams & Wilkins; 2010.
18. Kridis WB, Toumi N, Chaari H, et al. A review of Ewing sarcoma treatment: is it still a subject of
debate? Rev Recent Clin Trials. 2017;12(7):19–23 [Epub ahead of print. PMID:28117008].
1. Which primary bone malignancy is found almost exclusively in the axial

skeleton?
A. Osteosarcoma
B. Undifferentiated pleomorphic sarcoma
C. Chordoma
D. Ewing sarcoma
2. Which radiographic feature would be most likely to be present at initial

diagnosis in a 59-year-old man with osteosarcoma?
A. Rings-and-arcs calcifications
B. Cortical penetration
C. Sclerotic margin around the lesion
D. Pathologic fracture
3. Which primary bone malignancy is characteristically found in the tibial shaft?

A. Chondrosarcoma
B. Parosteal osteosarcoma
C. Adamantinoma
D. Undifferentiated pleomorphic sarcoma
4. Which radiographic feature is most characteristic of multiple myeloma?

A. Amorphous mineralization
B. Sclerotic margin
C. Layered periosteal reaction
D. Absence of reactive bone formation

1. C Chordoma is found almost exclusively in the sacrococcygeal region or the
clivus.
2. B At typical presentation, osteosarcomas have already penetrated the cortex
and extended into the soft tissues.
3. C Adamantinoma is found almost exclusively in the tibial shaft.
4. D Multiple myeloma lesions typically show an absence of reactive bone
formation.
14
Imaging of Musculoskeletal
Metastases
Felix S. Chew
This chapter describes the radiology of tumors that are metastatic to the
musculoskeletal system.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of metastatic musculoskeletal
tumors, the learner will be able to
4. summarize relevant concepts and knowledge for the following topics: incidence of metastases,
tumor spread, radiologic appearance, screening for metastases, pathologic fracture, soft-tissue
metastases, treatment, and radiotherapy changes.
INCIDENCE
More than 95% of adult patients with malignant disease involving bone have
metastases rather than myeloma or primary bone sarcomas.1,2 The prevalence of
bone involvement in autopsy series of patients with cancer ranges from 3% to
85%, depending on the site of origin and the thoroughness of the postmortem
search. With improving cancer treatments and longer patient survival, more and
more patients with cancer will have skeletal involvement by the end of their
clinical course. Most skeletal metastases occur in middle-aged and elderly
patients with primary cancers of the prostate, breast, lung, or kidney. In men,
prostate malignancies account for 60% of patients with skeletal metastases; in
women, breast malignancies account for 70% (Table 14.1). The relative
incidence of primary tumors that are likely to metastasize to bone may be
affected in the future by the rising incidence of lung cancer among women (due
to smoking), the decrease in the proportion of advanced breast cancers (due to
screening mammography), and the increasing incidence of breast and prostate
cancers overall (due to an aging population). Most skeletal metastases are
subclinical and asymptomatic. When symptomatic, they present as bone pain or
pathologic fractures. Bone pain ranges in severity from minimal to extreme and
intolerable, but skeletal metastases are themselves rarely a cause of death.
In the radiologic evaluation of metastatic bone tumors, less emphasis is
placed on complete anatomic delineation of individual lesions and more on
discovering sites of disease and planning and following the course of palliative
therapy. Assessing the risk of subsequent pathologic fracture may also be of
clinical importance. Sometimes, a skeletal metastasis is the initial presentation of
malignant disease in a patient whose primary site is asymptomatic or minimally
symptomatic. Occult primary tumors that present with bone metastases are
usually kidney, lung, and gastrointestinal tract lesions. Only in select cases does
locating the primary tumor benefit the patient, because in most instances, the
prognosis has already become unalterable by metastatic dissemination. In most
cases, the primary tumor is never located, even at autopsy. Biopsy of the skeletal
metastasis in these circumstances often shows adenocarcinoma without organ-
specific features.
TUMOR SPREAD
Tumor cells gain access to the skeleton by (1) hematogenous spread through the
arterial circulation, (2) retrograde venous flow, and (3) direct extension. The
portions of the skeleton that contain red marrow have a rich vascular supply, and
tumor emboli frequently lodge within the sinusoidal channels found there.
Tumor spread through retrograde venous flow occurs in the valveless vertebral
plexus of Batson. This venous plexus interconnects the spine, the ribs, and the
pelvis, providing access to the axial skeleton. Blood flow through the plexus
may be transiently reversed by increased intra-abdominal pressure caused by
activities such as coughing. Direct extension is much less frequent than
hematogenous spread; when it occurs, it is usually the extension of an
intrathoracic tumor to the chest wall, an intrapelvic tumor to the pelvic wall, or a
retroperitoneal process to the lumbar spine. For practical purposes, lymphatic
spread of tumor to bone does not occur.
Metastases in the cancellous bone of the axial skeleton and in the cancellous
metaphyseal bone of the proximal femur and proximal humerus account for
nearly 90% of lesions, a distribution that is related to hematogenous spread.
Metastases to the spinal column usually involve the vertebral body rather than
the posterior elements. They are more common in the lumbar region than the
thoracic region and least common in the cervical region. Metastases are
distinctly uncommon and distal to the knees or elbows. Approximately 90% of
patients with bone metastases have multifocal involvement.
Table 14.1 FREQUENCY OF PRIMARY SITES AMONG ADULTS WITH SKELETAL

METASTASES
Primary Site Frequency (%)

Women
Breast 70
Lung 6
Kidney 4
Uterus 4
Thyroid 3
Others/unknown 13
Total 100
Men
Prostate 60
Lung 14
Kidney 6
GI tract 3
Others/unknown 17
Total 100
Skeletal metastases are common around joints, especially the hips, shoulders,
knees, and intervertebral disks. Periarticular metastases with subchondral, intra-
articular, or synovial extension may have a clinical presentation that simulates
inflammatory arthritis. Lesions in the hands or feet are relatively rare and usually
come from primary lung cancers. The intervertebral disk is a relative barrier to
the spread of tumor, so that the usual pattern of vertebral metastatic involvement
is vertebral destruction with preservation of the disk, even when multiple
contiguous vertebral levels have tumor. It is very unusual for the disk to be
involved by tumor. Coexistent degenerative disk disease is frequent and may be
caused or exacerbated secondarily by the presence of tumor. In the subchondral
region of the vertebral body, a metastasis may interfere with the nutrition of the
disk or weaken the end plate so that the disk material herniates through. The
former process produces degenerative disk disease, and the latter produces a
Schmorl node.
RADIOLOGIC APPEARANCE
The appearance of a bone metastasis on radiographs reflects the balance of bone
destruction and bone formation. Metastatic tumors secrete osteoclast-stimulating
factors; the osteoclasts excavate a defect in the bone where the metastasis
establishes itself.3–5 The osteoclasts are not part of the tumor mass but can be
found at the periphery, sometimes separated by fibrous tissue. Growth of the
tumor is preceded by osteoclastic bone resorption. When bony trabeculae have
been completely engulfed, tumor can destroy the bone directly by elaborating
enzymes. Osteoclast proliferation and osteoclastic bone resorption occur in all
bone metastases, regardless of whether they also form bone. Bone formation
may occur as stromal bone formation or as reactive bone formation. In those
tumors associated with an acellular fibrous stroma, osteoprogenitor cells form
bone under the influence of osteoinductive humoral factors secreted by the
tumor. Metastases from prostatic carcinoma produce a fibrous stroma and form
bone in this way; metastases from breast and lung carcinomas do not. In reactive
bone formation, immature woven bone forms at the same time the bone
destruction occurs. Proposed mechanisms for reactive bone include a mechanical
response to weakening of the bone by the growing metastasis, an attempt by the
bone to contain the lesion, or perhaps an uncoupling of the humoral factors that
normally control bone formation and resorption.
•
FIGURE 14.1 Hypervascular renal cell carcinoma metastasis (arrow) destroying the
sternum and proximal left clavicle with large soft-tissue mass on axial CT.
Lytic lesions correspond to the destruction and replacement of bone by

nonmineralized tumor, often without appreciable bone formation.6 The pattern of
destruction may be geographic, permeated, or moth-eaten, and although there is
a rough correspondence to increasing biologic aggressiveness, all patterns may
be present in the same patient when extensive disease is present (Figures 14.1
and 14.2). Because 30% to 50% of the bone mineralization must be lost before a
lesion becomes visible on plain film, widespread lytic metastases may be
inapparent on radiographs. Blastic lesions correspond to bone formation in or
around tumor implants through reactive bone proliferation or ossification in
fibrous stroma.6 Reactive apposition of new bone on cancellous bone surfaces
results in a dense, blastic appearance. Proliferation of new endosteal bone is seen
as endosteal thickening or irregular densities projected over the marrow cavity.
Deposition of periosteal new bone causes cortical thickening or layers of
periosteal new bone. Metastatic lesions usually do not stimulate periosteal new
bone, and when they do, the periosteal bone tends to be scanty. The pattern of
reactive bone proliferation generally reflects the tumor’s growth rate, with highly
anaplastic, fast-growing tumors and marrow element malignancies (myeloma
and leukemia) provoking no radiographically appreciable reactive bone. Blastic
metastases tend to have a dense homogeneous appearance with margins that fade
imperceptibly into normal bone (Figures 14.3 and 14.4). Mixed lesions contain
both lytic and blastic areas, reflecting bone destruction and bone formation in
different portions of the same lesion (Figure 14.5). In fact, both processes occur
simultaneously in virtually all metastases.
The radionuclide bone scan is more sensitive than radiographs for detecting
metastases but has lower specificity. Radionuclide bone scanning agents such as
technetium-99m methylene diphosphonate accumulate in new reactive or
stromal bone (Figure 14.6). The metastasis itself may not accumulate the tracer
unless the primary lesion forms bone or cartilage. Most lytic lesions, as well as
all blastic and mixed lesions, have enough new bone formation to appear as
areas of intense uptake on scan. If the activity in the reactive and stromal bone is
equal to that of normal bone, or if the metastasis is in the marrow space but does
not affect the bone, the scan is falsely negative. If the bone is destroyed and
replaced by tumor without provoking detectable reactive bone, an area of
decreased uptake may result. Anaplastic, purely lytic lesions tend to have
decreased uptake. A “superscan,” that is, diffuse increased radionuclide
accumulation throughout the entire skeleton, can indicate diffuse osseous
metastatic disease.
•
FIGURE 14.2 Lytic metastases from breast carcinoma. A, Huge destructive lesion
(arrow) in the ilium. B, Lytic lesion (arrow) in the anterior two-thirds of the L3 vertebral
body.
•
FIGURE 14.3 Blastic metastases from breast carcinoma in the intertrochanteric
region of the femur. A, A homogeneously dense blastic lesion (arrow) with poorly
defined margins. B, Bone scan shows increased radionuclide accumulation in the
lesion (arrow) and in the ipsilateral acetabulum.
CT may show the extent of bone involvement more clearly than radiographs
(Figure 14.7). Delineation of the extent of cortical involvement is important
when prophylactic internal fixation is contemplated. In addition, CT may show
tumor in the marrow spaces in the absence of bone destruction. Increased
attenuation in the medullary cavity reflects replacement of fatty marrow by
tumor, edema, or reactive mesenchymal tissue (Figure 14.8).
On MRI, metastatic lesions are seen as focal areas of abnormal signal
replacing the normal marrow signal (Figure 14.9). Metastases are usually
distinguishable from normal tissue unless the metastases are so extensive that a
normal marrow signal is absent. On MRI, metastatic foci have low T1 signal,
high T2 signal, and enhancement. Opposed-phase MR sequences can be used to
assess for obliteration of the normal marrow fat, which is typically seen with
tumors. When fat and water are present in the same voxel, such as with red bone
marrow, then signal dropout will be seen on the out-of-phase image compared
with the in-phase image. Metastases obliterate the marrow fat, thus having
roughly the same signal intensity between in-phase and out-of-phase images
(Figure 14.10). MRI is more sensitive than bone scan and has superior anatomic
detail. MRI is the best examination for investigating acute spinal cord symptoms
in patients with known metastatic disease and for screening the spine when the
bone scan is negative and profound osteopenia is present (Figures 14.11 and
14.12). MRI may also be particularly helpful in making decisions about staging
and treatment when a solitary lesion is found on a screening bone scan and when
radiographs are normal.
Metastases may appear in any transverse or longitudinal location within an
involved bone, including marrow space, cortex, or surface, and epiphysis,
metaphysis, or diaphysis. Intracortical or subperiosteal locations are common for
metastases (Figures 14.13 and 14.14) but rare for primary bone tumors.
Positron emission tomography (PET) using 18-fluorodeoxyglucose (18-
FDG), a radioactive-labeled glucose analogue that permits imaging based on
metabolic rate, has considerable utility in oncologic imaging (Figure 14.15).
With regard to screening for skeletal metastases, compared with the radionuclide
bone scan, PET with 18-FDG appears to have higher sensitivity and higher
specificity for detection of osteolytic metastases.7,8 Osteoblastic metastases and
osteosarcoma metastases appear to have lower metabolic rates than osteolytic
metastases, and the radionuclide bone scan appears better than PET in these
circumstances. PET/CT has the additional advantage of combining the
sensitivity and specificity of PET with the spatial resolution of CT.
•
FIGURE 14.4 Diffuse blastic metastases from prostate carcinoma throughout the
pelvis and proximal femurs.
•
FIGURE 14.5 Metastasis from breast cancer detected by PET/CT. A, Axial CT
shows mixed lytic-sclerotic lesion (arrow) in the left iliac wing, adjacent to the
sacroiliac joint. B, Fused FDG PET/CT image shows high metabolic activity (arrow) in
the lesion. CT-guided biopsy confirmed the diagnosis.
•
FIGURE 14.6 Bone scan shows multiple metastases from breast carcinoma.
FIGURE 14.7 • Multiple blastic metastases from thyroid carcinoma on CT.
Radiographs and bone scan were normal.
•
FIGURE 14.8 Marrow space metastasis in the left femur (arrow) from lung cancer
demonstrated by CT. The bone scan was negative in the region of this lesion.
•
FIGURE 14.9 Metastases to the lumbar spine, pelvis, and femurs from breast
carcinoma. A and B, Coronal T1 and STIR MRIs show scattered, focal lesions in the
marrow.
•
FIGURE 14.10 Metastasis from lung carcinoma on axial T1 spoiled GRE MRI. A, In-
phase image shows a rounded lesion in the left sacrum (arrow) and heterogenous
marrow in the right ilium (arrowhead). B, Out-of-phase image demonstrates lack of
signal dropout of the metastasis (arrow) from lack of residual marrow fat and normal
signal dropout of the red marrow in the right ilium (arrowhead). Purely fatty replaced
marrow in the left hemipelvis is due to prior radiation and does not drop out because
of lack of interspersed cellular marrow elements.
•
FIGURE 14.11 Widespread spine metastases from breast carcinoma. A, Lateral
radiograph shows osteopenia and compression fractures in the thoracic spine. B,
Sagittal T2-weighted MRI shows widespread replacement of the normal marrow
signal by high-signal lesions.
•
FIGURE 14.12 Metastasis from colon carcinoma not evident on radiographs. A,
Composite sagittal T1 and STIR MRIs show replacement of the marrow at L3 (double
arrow) with low T1 signal and increased STIR signal. B, Posterior bone scan
demonstrates vague increased tracer uptake in L3 (arrow). C, CT before biopsy
demonstrates subtle sclerosis of the vertebral body.
•
FIGURE 14.13 Cortical metastasis. A, CT shows destructive lesion in the posterior
cortex of femur with irregular periosteal reaction (arrow). B, Axial T2 MRI shows the
lesion (arrow) with surrounding edema.
•
FIGURE 14.14 Femoral shaft metastasis in a 75-year-old man with history of lung
cancer. A, Anteroposterior radiograph of a femur shaft lesion with permeated
destruction. B, CT shows circumferential involvement. C, Axial FDG PET/CT fusion
image shows high metabolic activity in the lesion.
•
FIGURE 14.15 Metastatic osteosarcoma in a 26-year-old man undergoing routine
surveillance following treatment of osteosarcoma in the head and neck region. Iliac
wing lesion. A, Sclerotic lesion shown on attenuation-corrected CT. B, Fused axial
FDG PET/CT shows the lesion has intense glycolytic activity, characteristic for a
malignant tumor. Other portions of the examination documented additional bone
metastases with similar features (not shown).
•
FIGURE 14.16 Bone island in a 44-year-old woman with known metastatic disease.
A, CT shows small sclerotic lesion in the left ilium with morphologic features of bone
island. B, Fused axial FDG PET/CT shows no increased glycolytic activity in the
lesion, confirming bone island.
Common benign sclerotic bone lesions such as bone islands are frequently
discovered during staging studies and may mimic the appearance of sclerotic
metastases. Nuclear imaging may be helpful in these cases (Figure 14.16), as
may measurements of CT attenuation,9 but sometimes it is reasonable to perform
CT-guided biopsy.
SCREENING FOR METASTASES

Screening for skeletal metastases in patients with known primary malignancies is
often accomplished with bone scanning; 30% of metastatic lesions detected by
bone scan are missed by radiographs, and 2% of metastatic lesions detected by
radiographs are missed by scans. Because most patients have multiple lesions, it
is rare for a patient with osseous metastases to have an entirely normal bone
scan. The bone scan can be falsely negative or nondiagnostic in debilitated
patients with a poor host response or in patients who have had radiotherapy. In
patients with known primary malignancies and focal musculoskeletal symptoms,
it is reasonable to obtain radiographs as an initial screening examination for
metastatic disease. Some treatment protocols may be based on the burden of
disease as shown by radiographic osseous survey, despite the greater sensitivity
and specificity of other imaging modalities. Whole-body MRI, whole-body low-
dose CT, and whole-body PET/CT with FDG or other radiopharmaceuticals are
generally considered investigational but may be additional options.
PATHOLOGIC FRACTURE
Pathologic fractures through bones involved by metastases are common. The
most common sites of pathologic fracture are the vertebral bodies, ribs, pelvis,
proximal femur, and proximal humerus (Figures 14.17–14.19). Metastases of
lytic, blastic, and mixed radiographic appearance all cause weakening of the
bone.
•
FIGURE 14.17 Hand radiograph of a 64-year-old woman with destructive lesion and
pathologic fracture of her second metacarpal shaft from metastatic breast cancer.
In the spine, compression fractures with vertebral collapse occur, presumably

as a result of gradual destruction of the trabeculae that bear the compressive
loads. Involvement of the posterior elements may render some vertebral
fractures unstable. An epidural mass may be present and may block the spinal
canal. MRI or myelography with CT can demonstrate the epidural mass, indicate
the status of the spinal cord, and delineate the extent of vertebral disease.
In the long bones, destructive lesions with full-thickness cortical penetration
lead to pathologic fractures. Gaps in the cortex weaken the bone by causing
uneven and aberrant distribution of the stresses of loading, impeding the normal
biomechanical dispersion of force. Weakening is gradual as cortical bone is
infiltrated, eroded, and destroyed. Blastic lesions also destroy cortex, and the
reactive bone and stromal bone that give blastic lesions their radiodensity are
structurally unsound. The bone may fracture under the stresses of normal
activity. Cortical weakening makes bone most vulnerable to tensile forces;
therefore, in the long bones, pathologic fractures are usually transverse. The
onset of pain at a site of metastatic involvement may indicate the presence of
microfractures in a weakened cortex. Nontraumatic avulsion fractures about the
pelvis in adults are often pathologic.10
•
FIGURE 14.18 Pathologic fracture (arrows) transversely through lytic metastasis in
humeral shaft.
•
FIGURE 14.19 Prostate carcinoma with pathologic avulsion fracture of lesser
trochanter (long arrow). Brachytherapy seeds (short arrow) are present in the
prostate.
The goal of the treatment of osseous metastases is to palliate pain and prevent
pathologic fracture; curative resection is generally not realistic. Prophylactic
internal fixation of long bones with metastatic involvement is often considered.
The clinical decision revolves around the patient’s concerns and level of activity,
the localization and multiplicity of bone involvement, the extent of destruction,
and the patient’s life expectancy. Fixation is generally indicated for lytic lesions
if they are greater than 2.5 cm in size or involve more than half the
circumference of the bone. When pathologic fractures do occur, they are often
treated surgically. Prosthetic replacements allow the removal of the tumor-
destroyed bone. Bone cement is often used to buttress destroyed portions of the
bone and fill in bony defects. Radiotherapy can interfere with secondary healing
by destroying chondrogenesis. The primary osteogenesis that occurs with
internal fixation is more resistant to radiation, so that radiotherapy generally
does not interfere with the healing of internally fixed fractures. If the patient’s
life span is long enough, pathologic fractures will heal, but the healing process
may be prolonged. Median survival after discovery of a pathologic fracture
through an osseous metastasis, combined for all primary sites, is approximately
18 months.
SOFT-TISSUE METASTASES
Although the skeletal muscle mass of the human body accounts for a large
percentage of the total body weight, nearly 50%, in clinical experience, skeletal
muscle is an uncommon site for metastases.11–13 Muscle is resistant to both
primary and metastatic cancer. The cited factors for this resistance include
contractile activity, local changes in pH, oxygenation, accumulation of lactic
acid and other metabolites, blood flow per unit weight, intramuscular blood
pressure, and local temperature. Muscle metastases have been reported in sites of
previously documented skeletal muscle trauma.14
Autopsies in 2 series of patients showed that the prevalence of metastases to
muscle was 16.0% and 17.5%. Neoplasms with the highest incidence of
metastases to muscle were carcinoma, leukemia, and lymphoma. The diaphragm,
rectus muscle of the abdomen, deltoid muscle, psoas muscle, and intercostal
muscles were most commonly involved. The patients with muscle metastases
were 26 to 84 years old (mean age, 62 y). Most patients present with pain in the
involved muscles or a clinically palpable mass and have advanced-stage
neoplasms.
On unenhanced CT scans, a muscle metastasis may appear as simple
enlargement of a muscle. Occasionally, the findings may be subtle because the
tumor is isodense to the surrounding muscle, and contralateral asymmetry is
necessary to make the diagnosis. On contrast-enhanced CT, skeletal muscle
metastases appear as rim-enhancing intramuscular lesions with central
hypoattenuation (Figure 14.20). On MRI, muscle metastases have high T2
signal, lobulated morphology, large areas of central necrosis, and sometimes
extensive peritumoral edema (Figure 14.21). MRI findings of carcinoma
metastatic to muscle are not pathognomonic, and the differential diagnosis
generally includes soft-tissue sarcoma, hematoma, and abscess.
Metastases to skin, subcutaneous tissues, and lymph nodes may present as
soft-tissue masses. On CT, such lesions tend to be isodense to muscle and may
enhance (Figure 14.22). On MRI, soft-tissue metastases typically have low T1
signal, high T2 signal, and enhancement. A solitary soft-tissue mass is a very
unusual presentation of metastatic disease.15
TREATMENT
The basic treatment modalities for osseous metastases, with or without
pathologic fractures, are radiation therapy, chemotherapy, percutaneous image-
guided ablation, and surgical stabilization.16–20 Palliative radiation of
symptomatic lesions without pathologic fracture provides pain relief in
approximately 80% of patients. If a pathologic fracture is present, pain relief
may be experienced by approximately 60% of patients; without internal fixation,
the pathologic fractures may progress to nonunion.
Follow-up of osseous metastatic disease and screening for metastatic disease
after treatment response can be problematic, particularly in patients with breast
cancer. Osseous metastases that respond to treatment do so by infarction and
sclerosis. Lesions that were not sclerotic may become sclerotic in response to
treatment, so that a successful response may result in an increase in the number
of lesions visible on imaging (Figure 14.23). Because the sclerosis is a
metabolically active process, the lesion may continue to have abnormal features
on bone scan and PET/CT, and the features of the infarcted lesion itself may be
nonspecific on radiography, CT, and MRI. Thus, osseous metastatic disease with
a favorable response to treatment may have the same appearance on follow-up
exams as worsening metastatic disease that is not responding to treatment.
Percutaneous image-guided biopsy may be reasonable to perform in these
circumstances.
•
FIGURE 14.20 Soft-tissue metastasis from lung cancer. Contrast-enhanced CT
scan shows a rim-enhanced soft-tissue metastasis (arrow).
•
FIGURE 14.21 Metastases to muscle from lung cancer. A, Axial T2 FS MRI shows
high signal (arrow) in the lateral compartment muscles of the leg. B, Axial T1 FS Gd
MRI shows moderate enhancement (arrow) in the lesion.
•
FIGURE 14.22 Metastases from Merkel cell carcinoma. Enhanced axial CT shows
subcutaneous (short arrow) and intramuscular (long arrow) metastases.
•
FIGURE 14.23 Diffuse bone metastases from breast cancer. 32-year-old woman
with receptor-positive invasive ductal carcinoma. A-C, Axial T1, T2 FS, and T1 FS Gd
MRIs show multiple small lesions throughout the pelvis and sacrum. D, CT obtained
preparatory to needle biopsy showed no lesions, but the biopsy confirmed metastatic
disease. E, Follow-up CT after favorable response to systemic therapy shows multiple
small sclerotic bone lesions throughout the sacrum and pelvis. By imaging alone, it
cannot be determined if these are active lesions or not.
RADIOTHERAPY CHANGES
Therapeutic irradiation is a common means of treating osseous metastases.
Therapeutically irradiated osseous lesions heal by sclerosis and filling-in of lytic
areas. Radiation effects are independent of the radiation source.
In the mature skeleton, the primary change is radiation necrosis. This
osteonecrosis is dose-related. Radiographs and CT show irregular sclerosis in the
irradiated bone. Insufficiency fracture is a relatively common complication of
radiation necrosis (Figure 14.24). On bone scan, irradiated bone may initially
show increased radionuclide accumulation from hyperemia and new bone
formation. After several weeks or months, the bone scan shows decreased
radionuclide accumulation because of decreased bone formation and decreased
vascularity. On MRI, irradiated bone has the signal characteristics of fatty
marrow. The anatomic location and extent of these changes conform to the size
and shape of the radiation portal (Figure 14.25).
Malignant radiation-induced tumors may occur in older patients who have
received radiotherapy. The following criteria must be satisfied to make the
diagnosis of a radiation-induced sarcoma: (1) The sarcoma arises within the
irradiated field; (2) The latent period is at least 4 years; and (3) The sarcoma is
histologically different from a previous tumor, or the radiation was delivered in
the absence of a malignant diagnosis. The latent period averages 11 years. The
presence of pain, soft-tissue mass, and progression on serial films should raise
suspicion and lead to biopsy.
•
FIGURE 14.24 Insufficiency fractures (arrows) of the right ilium and right sacral
wing shown by coronal CT reformation in a patient with previous pelvic irradiation for
cervical cancer. Note the straight, vertical margins (small arrows) of the bilateral iliac
sclerosis, demarcating the margins of the radiation port.
Radiation myositis may occur following external beam radiation and is

manifested on MRI as muscle edema and inflammation that peaks several
months after treatment (Figure 14.26).21 The margins of the abnormality will
correspond to the radiation field and may extend straight across different muscle
groups and other soft tissues. Atrophy and volume loss are late effects of
radiation myositis.22
•
FIGURE 14.25 Radiation changes in marrow on sagittal T1 MRI. Fatty replaced
bone marrow in L2 and L4 (arrowheads) denotes the radiation portal surrounding a
lung carcinoma metastasis (arrow) at L3. The remainder of the levels has normal
marrow signal.
•
FIGURE 14.26 Radiation changes in muscle 6 months after treatment. A, Axial T1
MRI shows previous resection of soft-tissue sarcoma from the lateral portion of the
anterior compartment (arrow). B, Axial STIR MRI shows high signal in the lateral thigh
soft tissues, including muscle and subcutaneous tissues, with a linear demarcation
(arrows) that corresponds to the radiation portal. C, Axial T1 FS Gd MRI shows
enhancement (arrows) of the affected soft tissues.
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Roentgenol. 2001;178:423–427.
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2000;31:661–673.
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Roentgenol. 2002;178:985–988.
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1. What is the most common underlying malignancy in women with metastatic

bone disease?
A. Breast cancer
B. Thyroid cancer
C. Lung cancer
D. Colon cancer
2. What is the most common underlying malignancy in men with metastatic bone
disease?
A. Lung cancer
B. Thyroid cancer
C. Prostate cancer
D. Stomach cancer
3. In a patient with metastatic bone lesions, which of the following anatomic sites
is most likely to be involved?
A. Hand
B. Hip
C. Ankle
D. Foot
4. What is the most common mode of tumor dissemination that results in osseous
metastatic disease?
A. Direct extension
B. Lymphatic spread
C. Hematogenous spread
D. Iatrogenic implantation

1. A Breast cancer is the most common underlying malignancy with bone
metastases in women.
2. C Prostate cancer is the most common underlying malignancy with bone
metastases in men.
3. B Metastases to the proximal extremities are much more common than to the
distal extremities.
4. C Osseous metastatic disease is usually the result of hematogenous
dissemination.
15
Imaging of Soft-Tissue Lesions and
Calcifications
Felix S. Chew
Lumps and bumps are common clinical complaints involving the

musculoskeletal system. When further evaluation is necessary, imaging may be
appropriate.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of soft-tissue lesions and
calcifications, the learner will be able to
4. summarize relevant concepts and knowledge for the following topics: imaging methods, tumor
classification, soft-tissue sarcomas, lipoma, hemangioma, elastofibroma, peripheral nerve
sheath tumors, giant cell tumor of tendon sheath, aggressive fibromatosis, cysts and cystlike
lesions, myositis ossificans, calcific myonecrosis, chronic kidney disease-mineral and bone
disorder, primary tumoral calcinosis, muscular dystrophy, inflammatory myopathy, diabetic
myopathy, rhabdomyolysis, and accessory muscles.
IMAGING METHODS
Radiographs of suspected soft-tissue tumors are generally obtained first to
determine whether there is an underlying bone lesion. Sometimes, fat-containing
or mineralized lesions are recognized on radiographs. Cross-sectional imaging
with MRI, CT, or sonography may be obtained next, depending on the clinical
features and differential diagnosis. At the University of Washington, we favor
the routine use of MRI without and with gadolinium enhancement for lesions
thought to be deep-seated or solid. CT is often considered when lesions are
calcified. Sonography may be helpful in identifying cysts or vascular lesions and
for guiding percutaneous needle biopsy. Nuclear imaging with FDG-PET/CT
may be helpful in evaluating metastatic or recurrent disease but is generally not
used in the initial work-up because biopsy will be necessary almost regardless.
SOFT-TISSUE SARCOMAS
The annual incidence of soft-tissue sarcomas has been estimated at 50 per
million population. Approximately two-thirds of these are found in the
extremities and limb girdles (Table 15.1), making them more common than
primary bone sarcomas in the same regions. Most soft-tissue sarcomas present in
adults. Patients complain of a palpable mass of long duration and pain or
tenderness of insidious onset. Patients may delay seeking medical attention, and
this long chronicity may falsely suggest an indolent process. Most patients
present with lesions larger than 5 cm. Soft-tissue sarcomas metastasize
predominantly to lung, liver, or bone.
The World Health Organization classification of soft-tissue tumors, revised in
2013, is based on new knowledge from molecular genetics regarding the tissues
of origin of various tumors.1,2 The biological grade of soft-tissue sarcomas
depends on the degree of differentiation, the mitotic count, and the degree of
necrosis. Except for tumors containing gross fat, none of the several dozen types
of extremity soft-tissue sarcomas is radiologically distinctive. Indeed, the most
common extremity soft-tissue sarcomas are undifferentiated-unclassified
sarcomas: a category for sarcomas of undetermined tissue origin. These lesions
are typically pleomorphic, undifferentiated, and high grade and include lesions
that would have formerly been classified as malignant fibrous histiocytoma. Of
sarcomas of known origin, most are mesenchymal in origin and a minority are
neuroectodermal. In adults, the most common lesions are undifferentiated-
unclassified sarcomas, liposarcoma, synovial sarcoma, leiomyosarcoma, and
malignant schwannoma.3
Soft-tissue sarcomas often have nonspecific appearances on imaging, and
there are no reliable criteria for distinguishing among them by imaging (Figures
15.1–15.3). Factors that suggest sarcoma include older age, location in the thigh,
large size, round or ovoid shape, and involvement of adjacent bone. Larger
malignant soft-tissue masses usually have areas of inhomogeneity on MRI and
lower density on CT that correspond to regions of necrosis and hemorrhage, but
smaller lesions tend to be homogeneous. Sarcomas that frequently calcify or
ossify include synovial sarcoma (Figure 15.4), extraskeletal osteosarcoma, and
extraskeletal chondrosarcoma, but virtually any sarcoma may or may not have
calcification. The presence of fat within a lesion suggests a well-differentiated
liposarcoma (Figure 15.5), but higher-grade liposarcomas generally do not
contain radiologically identifiable fat. Small amounts of subcutaneous or
intermuscular fat may be engulfed by an aggressive sarcoma as it enlarges, so
that the presence of fat is not necessarily indicative of liposarcoma. On MRI,
soft-tissue sarcomas usually have intermediate T1 signal and high T2 signal.
Enhancement with intravenous contrast can be expected on both CT and MRI;
larger lesions tend to enhance heterogeneously, whereas smaller lesions tend to
enhance homogeneously. The goal of imaging, once the presence of the lesion is
confirmed, is to define the lesion’s size and location and the extent and anatomic
relation of the lesion to muscle compartments, fascial planes, neurovascular
bundles, and bone. Imaging-guided percutaneous biopsy has an important role in
diagnosis. The definitive treatment of soft-tissue sarcomas is surgical, sometimes
with neoadjuvant or adjuvant radiation therapy, chemotherapy, or both. Imaging
of soft-tissue sarcomas for surgical planning after neoadjuvant therapy may
reveal extensive areas of liquefaction, hemorrhage, and necrosis (Figure 15.6).
Five-year survival rates of 25% to 60% have been reported for extremity
sarcomas.
Table 15.1 ANATOMIC DISTRIBUTION SOFT-TISSUE SARCOMAS IN THE EXTREMITIES

AND LIMB GIRDLESa
Location Frequency(%)
Lower extremity 45
Upper extremity 16
Hip and buttocks 14
Proximal limb girdle 9
Foot and ankle 9
Hand and wrist 7
Based on Kransdorf MJ. Malignant soft- aBased on 6796 soft-tissue
tissue tumors in a large referral population: sarcomas of the
distribution of diagnoses by age, sex, and extremities and limb
location. AJR Am J Roentgenol. girdles, including all ages
1995;164:129–134. and all histologic types.
The AJCC prognostic stage groups for primary soft-tissue sarcoma of the
extremity and trunk depend on histologic tumor grade, tumor size, and
metastases (Table 15.2).4 Tumor size is measured as the greatest single
dimension in any plane. Low-grade tumors are stage I, with substages for tumor
size up to 5 cm (stage IA) or more than 5 cm (stage IB). High-grade tumors are
stage II for tumor size up to 5 cm, stage IIIA for tumor size more than 5 cm and
up to 10 cm, and stage IIIB for tumor size more than 10 cm. If regional nodal or
distant metastases are present, the lesion is stage IV, regardless of grade or size.
The Musculoskeletal Tumor Society surgical staging system may also be applied
to soft-tissue sarcoma (see chapter 11). Treatment decisions depend primarily on
whether the disease is localized or metastatic.
•
FIGURE 15.1 Undifferentiated pleomorphic sarcoma in a 58-year-old man with
medial thigh mass. A, Axial T1 MRI shows large subcutaneous mass with
intermediate signal. B, Axial T2 FS MRI shows heterogeneous high signal. C, Axial T1
FS Gd MRI shows diffuse enhancement except for the central region. D, Sonogram
shows heterogeneous solid mass. E, Core biopsy was performed.
•
FIGURE 15.2 Myxoid liposarcoma, low grade, in a 50-year-old man. A-C, Axial T1,
T2 FS, and T1 FS Gd MRI show a soft-tissue lesion in the anterior compartment
musculature of the left thigh. D, Sagittal T2 FS MRI. E, Axial CT. F, Sonography, long
axis, shows a solid heterogeneous lesion with regions of hypoechogenicity.
•
FIGURE 15.3 Primitive neural ectodermal tumor. Sagittal T1 MRI of the ankle
shows a lobulated soft-tissue mass in the posterior compartment.
Unlike sarcomas, which tend to respect anatomic planes and displace adjacent
structures as they enlarge, lymphoma may diffusely infiltrate throughout a
muscle, enlarging it, and spread across anatomic planes without displacing
structures (Figure 15.7; also see Figure 9.25).5 In other respects, imaging
features of lymphoma may be similar to other malignant soft-tissue lesions, with
intermediate T1 signal, high T2 signal, and enhancement.
BENIGN LESIONS
According to a large tumor registry,6 the most common benign mesenchymal
soft-tissue lesions are lipoma and lipoma variants (16%), fibrous histiocytoma
(13%), nodular fasciitis (11%), hemangioma (8%), fibromatosis (7%),
neurofibroma (5%), schwannoma (5%), and giant cell tumor of the tendon
sheath (4%).
Lipoma
Lipomas are common benign tumors consisting of mature fat. They are clinically
evident as soft, painless masses that gradually enlarge. Although most are
subcutaneous, they may occur in an intramuscular location. A definitive
diagnosis is made by CT when the lesion has the attenuation characteristics of fat
(Figures 15.8 and 15.9). Fat also has distinctive signal characteristics on MRI.
Unusual variants of soft-tissue lipomas that do not necessarily have detectable
fat on imaging include atypical lipoma and spindle cell lipoma (Figure 15.10).
•
FIGURE 15.4 Synovial sarcoma. A, Lateral radiograph of the knee shows a heavily
calcified mass (arrow) posterior to the knee. B, Axial T1 FS MRI following gadolinium
injection shows heterogeneous enhancement. The low-signal regions correspond to
calcification.
Hemangioma
Hemangioma is a benign vascular lesion that may contain nonvascular elements
such as fat, fibrous and myxoid tissue, smooth muscle, thrombus, and even bone.
Hemangiomas are classified histologically by the predominant type of vascular
channel (such as capillary, cavernous, arteriovenous, or venous). Hemangiomas
may be found in the subcutaneous tissue, within a muscle, or in a joint. At
radiography, hemangiomas appear as a nonspecific soft-tissue mass. Phleboliths
are seen in 30% of the hemangiomas, most frequently in cavernous
hemangiomas. CT reveals a soft-tissue mass with associated fat overgrowth and
serpentine vascular components, which may enhance after administration of
contrast. Sonography shows a complex mass with vascular channels, fat,
phleboliths, and blood flow. MRI is considered the best modality for evaluating
hemangiomas. Characteristic MRI features include lobulation, septation, central
low-signal-intensity dots, and marked enhancement after gadolinium
administration (Figure 15.11). The septated-lobulated appearance on T2 MRI
correlates with fibrous and fatty septa (low signal) between endothelial-lined
vascular channels (high signal). The central low-intensity dot sign on T2 MRI
may represent fibrofatty septa seen in cross section, hyalinized or thrombosed
vascular channels, smooth muscle components, fast flow within blood vessels,
calcification, or ossification.
Elastofibroma
Elastofibroma is a benign reactive fibrous lesion producing abnormal elastic
fibers.7 This pseudotumor is believed to result from chronic mechanical friction
between the tip of the scapula and the chest wall. An incidental prevalence of
2.0% was found in an elderly patient population studied by chest CT, but an
autopsy series found a frequency of 11.2% in men and 24.4% in women. The
characteristic location is between the chest wall and the inferior tip of the
scapula, but 5% of elastofibromas are found elsewhere. Most lesions are
asymptomatic, but patients may present with mass or pain. Large lesions may
ulcerate or cause brachial plexus impingement. Bilateral lesions are common but
are often asymmetric. On sonography, elastofibroma appears as arrays of
interspersed linear or curvilinear hypoechoic strands (elastic fibers) against an
echogenic background (entrapped fat). CT shows a mass of soft-tissue
attenuation with striations of fat attenuation (Figure 15.12). On MRI,
elastofibroma is a poorly circumscribed, semilunar, heterogeneous soft-tissue
mass with signal intensity similar to that of skeletal muscle interlaced with
strands of fat. Elastofibroma may have a marked enhancement after
administration of gadolinium. Surgery is curative; recurrences (7%) are probably
due to incomplete excision.
Giant Cell Tumor of Tendon Sheath

The extra-articular counterpart of pigmented villonodular synovitis, which is
histologically identical, is called giant cell tumor of the tendon sheath. This
lesion presents most commonly as a painless soft-tissue mass in the hand,
located along a tendon sheath. On radiographs, soft-tissue swelling may be seen.
On MRI, a soft-tissue mass with low to intermediate T1 signal and
heterogeneous high T2 signal is typical (Figure 15.13). An enhancement may be
seen on T1 FS Gd MRI. Giant cell tumor of the tendon sheath is not related to
giant cell tumor of bone.
Peripheral Nerve Sheath Tumors

Benign peripheral nerve sheath tumors (such as schwannoma and neurofibroma)
can arise from any central or peripheral nerve. They are usually found in young
adults between the third and fifth decades of life. Most are found incidentally,
but others, when large, may cause pain, soft-tissue mass, and neurologic
findings. They present as a fusiform soft-tissue mass related to the neurovascular
bundle (Figures 15.14 and 15.15). The affected nerve is seen entering and exiting
the mass. In neurofibroma, the nerve is central or obliterated by the mass. In
schwannoma, the nerve is eccentric to the mass, but this distinction may be
difficult to make on imaging. On T1 MRI, the split fat sign describes a rim of fat
around the tumor. On T2 MRI, the fascicular or target sign describes a ringlike
structure with central low-signal intensity and peripheral high-signal intensity.
Treatment is surgical excision.
•
FIGURE 15.5 Well-differentiated liposarcoma. A, Lateral radiograph of the thigh
shows a large, lucent lesion in the posterior soft tissues. B, Axial CT shows a
heterogeneous fat-containing soft-tissue mass in the posterior compartment of the
thigh. C, Axial T2 FS MRI shows high signal in some portions of the lesion with low
signal resulting from fat suppression in other portions of the lesion.
Neurofibromatosis type 1 has major musculoskeletal manifestations that

include scoliosis, mesodermal dysplasia, and neurofibromas (Figure 15.16).
Neurofibromas may erode adjacent bones and present as soft-tissue masses.
Aggressive Fibromatosis
Aggressive fibromatosis, also called desmoid tumor, is a true neoplasm of soft
tissues that arises from fascial and musculoaponeurotic coverings and may occur
anywhere those tissues are found. Sometimes, aggressive fibromatosis occurs at
the site of a traumatic or postsurgical scar. Nonencapsulated, poorly
circumscribed, and infiltrative, aggressive fibromatosis grows insidiously and
invades locally but does not metastasize. The lesion may grow large and become
adherent to neighboring structures such as neurovascular bundles. Aggressive
fibromatosis grossly resembles scar tissue. It is composed of well-differentiated
fibroblasts embedded in abundant collagenous matrix with increased cellularity
at the periphery. Radiographs may show soft-tissue mass, localized periosteal
thickening, and frank bony destruction. Because of variable degrees of
cellularity, matrix water content, and infiltration, aggressive fibromatosis may be
well or poorly defined and demonstrate variable attenuation and enhancement on
CT and variable signal intensity on MRI (Figure 15.17). The treatment is wide
resection and chemotherapy. Mortality is low, but local recurrences are frequent
(18%-54%).
FIGURE 15.6 • Preoperative staging for soft-tissue sarcoma in the anterior

compartment of the thigh after neoadjuvant therapy. A, Axial T2 MRI shows a tumor
(T) occupying the entire anterior compartment. Septation and stranding are present
within the lesion. B, Axial T1 FS MRI following gadolinium injection shows rim
enhancement (arrow), indicative of extensive necrosis of the nonenhancing regions.
Table 15.2 AJCC PROGNOSTIC STAGE GROUPS FOR PRIMARY SOFT-TISSUE

SARCOMA OF THE EXTREMITY AND TRUNK
Stage Grade Tumor Size Metastases

IA Low Up to 5 cm None
IB More than 5 cm
II High Up to 5 cm
IIIA More than 5 cm, up to 10 cm
IIIB More than 10 cm
IV Any Any Any
Based on Amin MB, Greene FL, Edge SB, et al, eds. AJCC Cancer
Staging Manual. 8th ed. New York: Springer; 2017:507–515.
CYSTS AND CYSTLIKE LESIONS

Synovial and Ganglion Cysts
Synovial cysts are fluid-filled juxta-articular masses. Unlike ganglia, synovial
cysts are lined by a synovial membrane that may or may not communicate with
the adjacent joint. The most common symptomatic synovial cyst is the Baker
cyst, found in the popliteal fossa. A Baker cyst results from distention of the
gastrocnemius-semimembranosus bursa by fluid from the knee joint. The fluid
enters through a slitlike communication with the posteromedial aspect of the
knee capsule—just above the joint line—between the tendons of the medial head
of the gastrocnemius and semimembranosus muscles. Baker cysts may be
associated with any condition in which there is a knee effusion, including
various forms of arthritis and various types of internal derangements. The most
common complication of a Baker cyst is rupture or dissection of fluid into the
adjacent gastrocnemius muscle belly, often resulting in a
pseudothrombophlebitis syndrome that mimics deep venous thrombosis of the
calf. On MRI, a ruptured Baker cyst may be recognized by the presence of fluid
extending from a Baker cyst or the site of a Baker cyst into the belly of the
medial gastrocnemius muscle or the adjacent calf or thigh muscles (Figure
15.18). A coexistent deep venous thrombosis may be present.
Ganglia are cystic nonneoplastic tumorlike lesions that are usually attached to
a tendon sheath, commonly found in the hands, wrists, and feet. They may also
be found near a joint, but some authors distinguish them from synovial cysts by
the lack of communication with a joint. Ganglia may be unilocular or
multilocular. MRI reveals a cystic mass with peripheral enhancement after
gadolinium. Sonography may characterize ganglia as cysts (Figure 15.19). When
large, ganglia may erode the adjacent bone, stimulate periosteal new bone
formation, cause compressive neuropathy, or rupture and leak.
Bursitis
Bursae are enclosed, flattened sacs consisting of synovial lining and a thin film
of synovial fluid. They facilitate motion between apposing tissues. Bursitis is
inflammation of the bursae due to trauma, repetitive stress, infection, or arthritis,
and the bursa may become distended with fluid as a result. In addition to normal
anatomic sites, adventitial bursae may develop at sites where there is movement
between apposing tissues. For example, bursae may develop over
osteochondromas or other bony prominences. Similar to bursae elsewhere,
adventitial bursae may become inflamed and cause symptoms. On imaging,
bursae appear as fluid-density masses in typical anatomic locations (Figure
15.20). They may show enhancement of the periphery or of septae on both CT
and MRI. Because gadolinium-based contrast diffuses into the extracellular
space, if there is sufficient delay between intravenous injection and imaging, a
bursa may enhance diffusely.
•
FIGURE 15.7 Intramuscular lymphoma. A, Axial T1 MRI shows a focal mass in the
medial head of the gastrocnemius muscle (arrow). The remainder of the
gastrocnemius muscle is atrophied (arrowhead). B, Axial T2 FS MRI shows high
signal in the mass (arrow).
•
FIGURE 15.8 Lipoma in the flexor aspect of the arm. A, Radiograph shows fat
lucency in biceps (arrow). B, CT shows fat within the lesion (arrow).
Myxoma
Myxomas are connective tissue tumors characterized by an abundant myxoid
matrix and a paucity of stromal cells. Myxomas may appear at any age. They
may be found in the subcutaneous tissue, within a muscle, or near a joint.
Intramuscular myxomas predominate in women in the fifth through seventh
decades of life and in the thigh. Intramuscular myxomas are well-circumscribed
cystic masses of homogeneous low T1 signal, high T2 signal, and peripheral and
septal enhancement after gadolinium. Intramuscular myxomas often have a
perilesional fat rind, corresponding histologically to atrophy of surrounding
muscle. Mazabraud syndrome is an unusual association of fibrous dysplasia with
intramuscular myxoma.
POSTTRAUMATIC MASSES
Hematoma and Morel-Lavallée Lesion
Soft-tissue hematomas are common after trauma. In most circumstances, the
diagnosis is apparent on clinical examination, but, occasionally, imaging may be
necessary to clarify the situation. Sonography at the point of care is often
available and easily incorporated into the clinical examination (Figure 15.21).
When the hematoma does not regress, an internal degloving injury may have
occurred with formation of a Morel-Lavallée lesion. Shear forces separate the
subcutaneous tissues from the underlying superficial fascia, resulting in a
potential space that fills with serous fluid, blood, or a combination of both.
Sometimes these collections become encapsulated and persistent (Figure 15.22)
and require surgical intervention.
•
FIGURE 15.9 Lipoma in the posterior thigh compartment. A, Axial T1 MRI shows
large fatty mass surrounded by muscle. The site of origin is difficult to determine. B,
Axial T2 FS MRI shows signal suppression in the mass similar to subcutaneous fat.
Myositis Ossificans
Myositis ossificans commonly refers to posttraumatic heterotopic ossification in
the muscles and other soft tissues after blunt trauma and hemorrhage. Most
common in the quadriceps muscles or around the elbow, it progresses over a few
weeks from hematoma to ill-defined calcification to well-organized cortical and
trabecular bone. The process is similar to the formation and maturation of
fracture callus and may be initially confused with sarcoma (Figure 15.23).
However, myositis ossificans evolves over a period of weeks into an organized,
peripherally calcified mass as it begins to ossify. The ectopic bone may
ultimately blend with underlying bone, sometimes causing mechanical problems.
Myositis ossificans may complicate acute or chronic bony or soft-tissue trauma
and may occur in association with neurologic diseases of a wide variety,
including paralysis and coma. A localized form that occurs without a history of
significant trauma is called myositis ossificans circumscripta. Treatment is rarely
indicated.
Calcific Myonecrosis
Calcific myonecrosis typically presents as an incidental large amorphous
fusiform calcification in the anterior compartment of the leg, the likely sequela
of anterior compartment syndrome, myonecrosis, and dystrophic calcification
(Figure 15.24).8 Patients will have foot drop and the appropriate history. This
appearance in this location is virtually pathognomonic, but calcific myonecrosis
has been reported in other sites, including other compartments of the leg, the
forearm, and the thigh.
SOFT-TISSUE CALCIFICATION
Chronic Kidney Disease-Mineral and Bone Disorder
Chronic kidney disease-mineral and bone disorder is a term that includes various
musculoskeletal manifestations of renal failure. The bone aspect of this
condition, renal osteodystrophy, is described in chapter 24. Soft-tissue
calcification in chronic kidney disease is common (Figure 15.25) and often
reflects hypercalcemia, abnormal calcium-phosphorus metabolism, and local
tissue effects. Sometimes referred to as metastatic calcification when
widespread, it is often seen in arteries and in the subcutaneous, tenosynovial, and
periarticular soft tissues. When large, calcium deposits may erode adjacent bone.
Large tumorlike soft-tissue deposits of hydroxyapatite around joints (dialysis-
related tumoral calcinosis) may be found in patients on dialysis for chronic renal
failure (Figure 15.26). Because the crystals are often aqueous suspensions (milk
of calcium), CT and upright radiographs may demonstrate fluid-sediment levels.
The calcification may be difficult to detect on MRI sequences because the
calcified collections are of low signal and isointense to the involved tendons.
MRI may show muscle and soft-tissue edema associated with the calcifications.
These deposits may temporarily regress with dialysis.
Primary Tumoral Calcinosis

Primary tumoral calcinosis, as distinguished from dialysis-related tumoral
calcinosis, is an uncommon disorder characterized by accumulations of calcium
hydroxyapatite crystals in the periarticular soft tissues with granulomatous
reaction.9 An inborn error in phosphorus metabolism is thought to be the cause
of these nonneoplastic lesions; approximately one-third of reported cases are
familial. The masses tend to grow slowly over many years to a large size;
symptoms may be caused by their physical bulk. Most are discovered in the first
or second decade of life. These accumulations are composed of multiple
globules of calcification separated by radiolucent bands. Fluid levels are usually
present but may not be evident except on CT (Figure 15.27). The lesions are
frequently found in the normal location of bursae. The treatment is surgical, but
local recurrences are not uncommon.
•
FIGURE 15.10 Spindle-cell lipoma. A-C, Axial T1, STIR, and T1 FS Gd MRI show
an ovoid lesion in the posterior arm musculature (arrow) with no distinctive features.
D, Sonogram shows heterogenous solid lesion. Percutaneous biopsy was performed.
MUSCLE CONDITIONS
Muscular Dystrophy
Muscular dystrophy comprises a heterogenous group of genetic diseases
characterized by progressive atrophy of skeletal muscle. Depending on the
particular genetic defect and its expression, age of onset, anatomic distribution,
severity, rate of progression, and pattern of inheritance vary among the different
types of muscular dystrophy, dozens of which have been described. Radiologic
features of muscular dystrophy in the musculoskeletal system include fatty
replacement of muscles, usually symmetric and diffuse (Figure 15.28), and if the
onset is during skeletal maturation, dysplastic bone changes. Multisystem
manifestations may also be present in some forms of muscular dystrophy.
Inflammatory Myopathy
The idiopathic inflammatory myopathies are a heterogeneous group of muscle
diseases of unknown cause. An autoimmune process is involved, but as with
many other autoimmune diseases, the triggers are unknown. Some inflammatory
myopathies are inherited. Inclusion body myopathy is an inflammatory
myopathy in which distinctive inclusion bodies are found in muscle fibers on
biopsy. Patients have progressive muscle weakness of gradual onset, typically
wrists, fingers, and thighs. Older adults are affected, men more than women.
MRI may demonstrate muscle edema and fatty atrophy (Figure 15.29).10
•
FIGURE 15.11 Intramuscular hemangioma. A, Coronal T1 MRI of the thigh shows a
heterogeneous fatty lesion (arrow) in vastus medialis. B, Coronal inversion recovery
MRI shows serpiginous structures with high signal (arrow).
•
FIGURE 15.12 Elastofibroma dorsi of the chest wall. Axial CT of the chest reveals
right subscapular soft-tissue mass (arrow) applied to the chest wall with striated
appearance caused by alternating bands of soft tissue and fat attenuation.
Diabetic Myopathy
Diabetic myopathy occurs in patients with both type 1 and type 2 diabetes. It is
thought to result from microvascular insufficiency and may occur with other
comorbidities of longstanding, poorly controlled diabetes. Acute muscle
ischemia, inflammation, and infarction may present abruptly with pain,
tenderness, or swelling, similar to infection. Although diabetic myopathy is
typically a self-limited process that resolves spontaneously, myonecrosis may
result. The anterior compartment of the thigh and the posterior compartments of
the leg are the most frequently involved sites. On MRI, the condition is evident
as diffuse muscle enlargement and high T2 signal in the regions of involvement;
subcutaneous edema and subfascial fluid are usually present (Figure 15.30).
Regions of high T1 signal may indicate hemorrhage, and rim enhancement
following gadolinium would suggest muscle infarction and necrosis.11
Rhabdomyolysis
Rhabdomyolysis is the condition in which damaged skeletal muscle breaks down
rapidly, releasing muscle breakdown products such as myoglobin and creatine
kinase into the soft tissues and bloodstream. There are various underlying causes
of the damage, including trauma, strenuous exercise, ischemia, drugs, and
infection. Compartment syndrome, disseminated intravascular coagulopathy, and
renal failure are potential complications of rhabdomyolysis. On MRI, muscle
edema and swelling may be seen (Figure 15.31).12
Accessory Muscles
There may be considerable normal variation in muscle anatomy. Occasionally,
accessory muscles or other anomalies may present as or be confused with soft-
tissue tumors. The origins of the medial and lateral heads of the gastrocnemius
are variable, and in some instances, an anomalous origin may entrap the
popliteal artery and present as a popliteal mass (Figure 15.32). There are
multiple accessory muscles that may occur at the ankle. The most common and
robust of these muscles is the accessory soleus, which may occupy Kager fat pad
between the Achilles tendon and the posterior tibia (Figure 15.33).
0
•
FIGURE 15.13 Giant cell tumor of tendon sheath. A, Anteroposterior radiograph
shows a focal soft-tissue mass along the medial aspect of the first metatarsal head. B,
Axial T2 FS MRI shows lobulated morphology and high signal within the lesion. C,
Coronal T1 MRI shows low signal within the mass. The mass erodes the tibial
sesamoid (arrow).
•
FIGURE 15.14 Schwannoma (different patients). A, Sciatic nerve schwannoma
(arrow) shown by sagittal T1 MRI. B, Tibial nerve schwannoma with high signal
(arrowhead) surrounding a lower signal center (arrow), the target sign, shown by axial
T2 MRI.
•
FIGURE 15.15 Neurofibroma in a 28-year-old woman with left sciatica. A, Axial T1
MRI shows a large soft-tissue mass occupying the right sciatic notch anterior to the
piriformis and extending across the midline. The visceral structures have been
displaced. B, Axial T2 FS MRI shows heterogenous high signal within the mass. C,
Axial T1 FS Gd MRI shows heterogeneous enhancement.
•
FIGURE 15.16 Neurofibromatosis in an adult. A, Axial T1 MRI shows multiple
lobulated soft-tissue mass in and around the right buttock with dysplastic underlying
bone and muscle atrophy. B, Axial T2 MRI shows high signal within the masses.
FIGURE 15.17 • Recurrent aggressive fibromatosis. Axial T2 FS MRI shows
irregularly shaped mass involving the teres major and latissimus dorsi at the site of
previous resection for aggressive fibromatosis.
•
FIGURE 15.18 Baker cyst in a 45-year-old woman with posterior knee swelling. A,
Transverse sonogram shows well-circumscribed anechoic, avascular fluid-filled
structure. B, Longitudinal sonogram shows the lesion between the medial head of the
gastrocnemius (long arrow) and semimembranosus muscles (short arrow).
•
FIGURE 15.19 Ganglion cyst in finger. A and B, Transverse and longitudinal
sonograms of the volar proximal middle finger show a small well-circumscribed
anechoic avascular fluid-filled structure (arrows) superficial to the flexor tendons.
•
FIGURE 15.20 Cubital bursitis causing swelling in the antecubital fossa. A, Axial T1
MRI shows intermediate signal mass surrounding the brachialis tendon; note skin
marker. B, Axial PD FS MRI shows the mass is a fluid-filled septated bursa. C, Axial
T1 FS Gd MRI shows enhancement of the periphery and septa.
•
FIGURE 15.21 Posttraumatic subcutaneous hematoma. A, Anteroposterior knee
radiograph shows mild medial soft-tissue swelling. B, Sonogram shows
heterogeneous complex fluid collection without vascularity in the area of swelling.
•
FIGURE 15.22 Morel-Lavallée lesion (internal degloving injury) in a 47-year-old
woman whose knee was rolled over by a car 4 weeks earlier. A, Coronal T1 MRI
shows extensive lesion (arrow) in the medial subcutaneous tissues with high and low
signal, consistent with hemorrhage. B, Axial STIR MRI shows multiple fluid-fluid levels
within the lesion.
•
FIGURE 15.23 Myositis ossificans in a 60-year-old man who presented with a new
deep soft-tissue mass in the thigh. A, At onset, axial T2 FS MRI shows large masslike
lesion in the anterior thigh compartment involving the vastus intermedius. The lesion
has heterogenous high signal and circumferential organization around the femur. The
lesion was 19 cm long in the craniocaudal dimension (not shown). B, 5 months after
onset, axial T2 FS MRI shows marked diminution in size of lesion. C, 7 months after
onset, axial T2 FS MRI shows further diminution. D, Axial CT shows mature soft-
tissue ossification (arrow).
FIGURE 15.24 • Calcific myonecrosis. A and B, Lateral and anteroposterior
radiographs of the leg show large plaquelike calcification in the anterior compartment
of the leg. C, Axial CT shows diffuse calcification of the lesion with foci of very dense
calcifications.
FIGURE 15.25 • Metastatic calcification diffusely distributed in the skin and

subcutaneous tissues of a patient with end-stage renal disease. A, Anteroposterior
•
FIGURE 15.26 Periarticular calcinosis in a patient on hemodialysis for chronic renal
failure. A, Radiograph shows calcium deposits around the hip (long arrow) and gluteal
musculature (short arrow). B, Axial CT shows fluid-fluid levels (arrow) within the
calcium deposits.
•
FIGURE 15.27 Idiopathic tumoral calcinosis. A, Anteroposterior radiograph shows
amorphous multilobular calcifications. B, Axial T1 MRI shows low-signal calcifications.
•
FIGURE 15.28 Limb girdle muscular dystrophy in an adult. Oblique coronal T1 MRI
shows fatty replacement of all the shoulder muscles.
•
FIGURE 15.29 Inclusion body myositis in a 54-year-old man with progressive
weakness. A, Axial T1 MRI through both thighs shows extensive, symmetric fatty
replacement of most of the thigh musculature. B, Axial STIR MRI shows that a few
regions of the anterior quadriceps musculature show increased signal.
•
FIGURE 15.30 Diabetic myopathy in a 41-year-old man with sudden onset of thigh
swelling but no signs of infection. A, Axial T2 FS MRI shows abnormal high signal in
the anterior compartment, involving predominantly the vastus medialis (arrow). There
is subcutaneous edema and subfascial fluid. B, Axial T1 FS MRI shows regions of
abnormal high signal (arrow) and mild mass effect in the vastus medialis. C, Coronal
STIR MRI shows the cranial and caudal extent of the muscle involvement.
•
FIGURE 15.31 Rhabdomyolysis. Intravenous drug user who inadvertently injected
the femoral artery instead of the femoral vein. A and B, Coronal and axial STIR MRI
show marked muscle edema involving portions of the anterior, adductor, and posterior
compartments of the thigh from acute embolic ischemia resulting in rhabdomyolysis.
FIGURE 15.32 • Popliteal artery entrapment syndrome. Bilaterally symmetric
anomalous medial heads of the gastrocnemius muscles (arrows) fill the popliteal
fossae, displacing the popliteal neurovascular structures laterally. The patient was
originally referred for popliteal fossa masses.
•
FIGURE 15.33 Accessory soleus (different patients). A, Lateral radiograph shows
an elongated structure (S) filling the Kager fat pad and tapering as it approaches the
calcaneus. B, Axial CT shows the accessory muscle (arrow) between the tibia and the
Achilles tendon.
References
1. Baheti AD, O’Malley RB, Kim S, et al. Soft-tissue sarcomas: an update for radiologists based on the
revised 2013 World Health Organization classification. AJR Am J Roentgenol. 2016;206(5):924–932.
doi:10.2214/AJR.15.15498 [Epub March 21, 2016. PMID:26998884].
2. Fletcher C, Bridge J, Hogendoorn P, Mertens F, eds. World Health Organization Classification of
Tumours of Soft Tissue and Bone: Pathology and Genetics of Tumours of Soft Tissue and Bone. 4th ed.
Lyon: IARC Press; 2013.
3. Kransdorf MJ. Malignant soft-tissue tumors in a large referral population: distribution of diagnoses by
age, sex, and location. AJR Am J Roentgenol. 1995;164(1):129–134 [PMID:7998525].
4. Amin MB, Greene FL, Edge SB, et al., eds. AJCC Cancer Staging Manual. 8th ed. New York: Springer;
2017:507–515.
5. Surov A. Imaging findings of skeletal muscle lymphoma. Clin Imaging. 2014;38(5):594–598.
doi:10.1016/j.clinimag.2014.03.006 [Epub March 22, 2014. PMID:24735681].
6. Kransdorf MJ. Benign soft-tissue tumors in a large referral population: distribution of specific diagnoses
by age, sex, and location. AJR Am J Roentgenol. 1995;164(2):395–402 [PMID:7839977].
7. Battaglia M, Vanel D, Pollastri P, et al. Imaging patterns in elastofibroma dorsi. Eur J Radiol.
2009;72(1):16–21. doi:10.1016/j.ejrad.2009.05.024 [Epub June 17, 2009. PMID:19539441].
8. O’Dwyer HM, Al-Nakshabandi NA, Al-Muzahmi K, Ryan A, O’Connell JX, Munk PL. Calcific
myonecrosis: keys to recognition and management. AJR Am J Roentgenol. 2006;187(1):W67–W76
[PMID:16794141].
9. Olsen KM, Chew FS. Tumoral calcinosis: pearls, polemics, and alternative possibilities. RadioGraphics.
2006;26(3):871–885 [PMID:16702460].
10. Mulcahy H, Chew FS. MRI of nontumorous skeletal muscle disease: case-based review. AJR Am J
Roentgenol. 2011;196(6 suppl):S77–S85. doi:10.2214/AJR.09.7186 [PMID:21606237].
11. Huang BK, Monu JUV, Doumanian J. Diabetic myopathy: MRI patterns and current trends. AJR Am J
Roentgenol. 2010;195:198–204.
12. Wang EC, Chew FS. MR findings of alprazolam injection into the femoral artery with
microembolization and rhabdomyolysis. Radiol Case Rep. 2015;1(3):99–102. doi:10.2484/rcr.v1i3.33
[eCollection 2006. PMID:27298694; PMCID:PMC4891562].
1. Which soft-tissue lesion is most likely to show perilesional edema on T2 FS

MRI?
A. Undifferentiated pleomorphic sarcoma
B. Intramuscular abscess
C. Tumoral calcinosis
D. Intramuscular lipoma
2. Which soft-tissue lesion is most likely to show heterogeneous enhancement on

T1 FS Gd MRI?
A. Undifferentiated pleomorphic sarcoma
B. Intramuscular abscess
D. Intramuscular lipoma
3. Relatively rapid changes in size are typical of which of the following soft-
tissue lesions?
A. Giant cell tumor of tendon sheath
B. Intramuscular lipoma
C. Elastofibroma
D. Dialysis-related tumoral calcinosis
4. Which of the following conditions is most closely associated with extremity

compartment syndrome?
A. Chronic kidney disease-mineral and bone disorder
B. Aggressive fibromatosis
C. Rhabdomyolysis
D. Inflammatory myopathy

1. B Perilesional edema is typical of inflammatory but not neoplastic lesions.
2. A Soft-tissue sarcomas typically enhance heterogeneously.
3. D Dialysis-related tumoral calcinosis may change rapidly in size in response
to dialysis.
4. C Among the options, rhabdomyolysis is most closely associated with
compartment syndrome.
16
Imaging Basics of Arthritis
Michael L. Richardson
In the ensuing pages, I will describe my own personal system for the diagnosis
of arthritis.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging basics of arthritis, the learner will be
able to
4. summarize relevant concepts and knowledge for the following topics: approach to diagnosing
arthritis, the Sutton law, osteophyte formation, chondrocalcinosis, erosions, soft-tissue swelling,
typical and atypical patterns of involvement, demographics of arthritis, and application of
Occam’s razor and Hickam’s dictum in diagnosis.
APPROACH TO DIAGNOSIS
The radiology of arthritis is essentially the radiology of osteoarthritis and other
forms of joint degeneration. In fact, osteoarthritis is my diagnosis in roughly
95% of the joint images I interpret. This is true even though I work at a large
tertiary care center, where potentially any known arthropathy might spring up.
Because of this overwhelming prevalence of osteoarthritis, a radiologist
preparing for a life of interpreting joint images should therefore spend most of
his/her time studying osteoarthritis and its many manifestations. This is a
powerful concept in the workup of joint pain. If one were to ignore the images
and any other history and blindly dictate “osteoarthritis,” preceded by some
modifying term (ie, “no,” “mild,” “moderate,” or “severe”), one would be right
more than 95% of the time. I do not know any radiologist who works this way. I
approach each joint examination with the thought that “this is probably
osteoarthritis, but…” and then look carefully for any findings that should steer
me away to some other arthropathy. My personal approach to the diagnosis of
arthritis is to consider the following 5 factors: the Sutton law, radiographic
hallmarks, pattern approach, demographics, and the law of parsimony versus
Hickam’s dictum. I initially put this list together as a simple tool for teaching
residents about arthritis. However, after several decades of interpreting joint
images, I find that they work pretty well for me too.
RULE 1: THE SUTTON LAW

Medicine has come a long way since its early days, when any type of joint
disease was simply called “rheumatism.” We now recognize more than 100
different causes of arthritis1 and have summarized many of them in Table 16.1.
As I suggested in the introduction, 95% of the arthritis cases one sees are
osteoarthritis or some other degenerative joint disease. If we consider 2 more
entities, we can create a short list that should extend our diagnostic coverage to
more than 99%. This short-list approach to diagnosis can be considered a form
of the Sutton law. This law has been ascribed to Willie Sutton, a bank robber
famous in the early 20th century. When asked why he robbed banks, he
reportedly said, “Because that’s where the money is.”2 For radiologists, the
“money” represents the correct diagnosis. In the appendicular skeleton, the
money usually lies in one of what one might call “the Big Three” (Table 16.2).
This same differential is seen in the axial skeleton. The main differences are that
we must consider a new type of joint—the intervertebral disk joint—and we
must also include several spondyloarthropathies in our differential (Table 16.1).
RULE 2: RADIOLOGIC HALLMARKS

At this point, the Sutton law has given us a short differential diagnosis that
should contain the actual diagnosis about 99% of the time. Now it is time to
actually look at the images. We would like to answer 2 key questions as we do
this: (1) What kind of arthropathy does the patient have? (2) How bad is it?
There are imaging findings common to many forms of arthritis (Table 16.3).
However, most of these findings are nonspecific. Joint space narrowing, for
example, is an important finding to note on a radiograph, as it is an index of the
severity of the patient’s disease. Unfortunately, it tells you nothing about what
they have. Just about any arthropathy that damages cartilage (and that would be
most of them) will result in joint space narrowing. In the interests of diagnostic
efficiency, it therefore makes sense to first look for the findings that will quickly
tell us what the patient has, ie, the most specific findings. As it turns out, there
are 3 findings on that list that are fairly specific. Each of these “hallmark”
findings is specific for 1 of the 3 types of arthritis we considered with the Sutton
law (Table 16.4).
Table 16.1 SOME OF THE RECOGNIZED FORMS OF ARTHRITIS
Autoinflammatory diseases
Avascular necrosis
Crystal-associated arthropathies
Heritable disorders of connective tissue
Infection-associated rheumatic syndromes
Inflammatory myopathies and other muscle disorders
Metabolic bone disorders
Osteoarthritis and related conditions
Posttraumatic arthritis
Relapsing polychondritis
Rheumatic diseases of childhood
Rheumatic manifestations of systemic disease
Rheumatoid arthritis
Sjögren syndrome
Soft-tissue rheumatic syndromes
Spondyloarthropathies
Systemic lupus erythematosus
Systemic sclerosis and related conditions
Tumor-associated rheumatic syndromes
Vasculitis
Table 16.2 THE BIG THREE DIAGNOSES
Appendicular
Category Skeleton Axial Skeleton
Degenerative Osteoarthritis Facet osteoarthritis, disk
degeneration, diffuse idiopathic
skeletal hyperostosis
Depositional Usually Usually pyrophosphate arthropathy
pyrophosphate
arthropathy but
occasionally gout
Inflammatory Rheumatoid Spondyloarthropathy (ankylosing
arthritis spondylitis, psoriatic arthritis,
reactive arthritis, and inflammatory
bowel disease)
Table 16.3 FINDINGS COMMON TO MANY FORMS OF ARTHRITIS
Joint space narrowing

Osteophytosis
Subluxation
Dislocation
Ankylosis
Erosions
Soft-tissue swelling
Chondrocalcinosis
Subchondral sclerosis
Subchondral cysts
Table 16.4 HALLMARK RADIOLOGIC FINDINGS
Appendicular
Category Skeleton Axial Skeleton
Degenerative Osteophytes Osteophytes, disk space
narrowing
Depositional Chondrocalcinosis Chondrocalcinosis
Inflammatory Erosions Erosions, syndesmophytes
Osteophyte Formation
An osteophyte is one of the most specific findings seen in joint imaging. An
osteophyte at the margin of a diarthrodial joint (ie, a “marginal” osteophyte) is
virtually pathognomonic for osteoarthritis (Figure 16.1).3,4 In the spine,
osteophytes are commonly seen at the margins of the vertebral bodies, because
of disk degeneration.5 However, there are other osteophytes that have nothing to
do with osteoarthritis. Osteophytes can also form at entheses—the spots where
ligaments and tendons attach to the bone (Figure 16.2).6 Usually, this type of
osteophyte is seen in an area of altered or increased stress at the enthesis (ie, a
“traction” osteophyte) (Figure 16.3). However, enthesophytes may also form in
response to inflammation (syndesmophytes), as well as endocrine, metabolic, or
traumatic causes.
Chondrocalcinosis
The presence of crystal deposits (chondrocalcinosis or tophi) indicates one of the
crystalline arthropathies. In calcium pyrophosphate dihydrate (CPPD) deposition
disease, the most common site of radiographic calcifications is in the
fibrocartilage and hyaline articular cartilage (chondrocalcinosis) (Figures 16.4
and 16.5).7–9 However, calcifications may also be seen in the joint capsule or
synovial membrane. Calcifications may occasionally be seen in gouty tophi.
Erosions
In general, the presence of erosions bespeaks some type of inflammatory
disease, whether the erosions are due to synovial hypertrophy, crystalline
deposits, or infection. In rheumatoid arthritis (RA), the erosions follow the
development of an inflammatory proliferation of the synovium, called pannus.
As this pannus increases in amount, it begins to cause erosions of the chondral
surface and at the periarticular “bare” areas (Figure 16.6).10,11 These bare areas
refer to the bone within the synovial space, which is not covered by articular
cartilage. The articular cartilage offers relative protection to the bone that it
covers. The marginal bare areas are not covered by cartilage, and the earliest
erosions of RA can be seen here (Figures 16.7 and 16.8). If the inflammation
proceeds unchecked, the erosions of the bone and the cartilage may become
profound, and the joint may finally undergo fibrous ankylosis. In gout, erosions
are caused by tophi.12,13 These tophi may be either intra- or extra-articular in
location and may appear similar to those seen in RA (Figure 16.9). However, in
gout, there tends to be early sparing of the articular cartilage between the
erosions, whereas the cartilage is thinned much earlier in the course of RA.
Soft-Tissue Swelling
Soft-tissue swelling at a joint may reflect capsular distention from effusion,
synovial hypertrophy, soft-tissue edema, or a mass. Symmetric, fusiform
swelling suggests an inflammatory process with effusion, synovial edema,
synovial hypertrophy, or some combination thereof (Figure 16.10). Inflammatory
distention of a tendon sheath may also produce soft-tissue swelling, but the
swelling extends beyond the joint. In a digit, this kind of swelling produces an
appearance that has been likened to a sausage because of the lack of contours
(sausage digit). Generalized soft-tissue swelling may be caused by subcutaneous
edema or hyperemia and suggests inflammation (Figure 16.11). Lumpy-bumpy
swelling that is not symmetric or centered near a joint suggests masses and may
be caused by metabolic deposition diseases with masslike deposits of metabolic
products in the periarticular soft tissues (Figure 16.12). Soft-tissue prominences
at joints may reflect bony or cartilaginous enlargement; for example, Heberden
and Bouchard nodes result from osteophyte formation at the distal
interphalangeal and proximal interphalangeal (PIP) joints of the hand,
respectively.
•
FIGURE 16.1 Prominent osteophytes are present at the distal interphalangeal joints
of the index (long arrow) and middle (short arrow) fingers, and the proximal
interphalangeal joint of the small finger (arrowhead). Smaller osteophytes are present
at the remaining interphalangeal joints. A, Lateral radiograph. B, Posteroanterior
radiograph.
•
FIGURE 16.2 Anatomy of an enthesis.
Other Findings
Other findings, such as joint space narrowing, subchondral cyst formation,
sclerosis, ankylosis, or subluxation, are not especially specific and may occur in
a wide variety of degenerative or inflammatory disorders in the appendicular
skeleton. It is important to describe these findings, because they tell us a lot
about the severity of the patient’s disease. However, they do not tell us much
about what specific disease is causing them.
•
FIGURE 16.3 A traction spur (enthesophyte) at the proximal olecranon (arrow).
RULE 3: PATTERN APPROACH

Certain arthropathies strike certain specific combinations of joints. The reasons
for these predilections remain obscure, requiring us to memorize empirical
patterns of joint involvement for the major arthropathies. Such empirical patterns
have been described for most of the appendicular joints.4,10,14 The most specific
patterns of joint involvement are seen in the hands and wrists (Figures 16.13 and
16.14). The findings of primary (idiopathic) osteoarthritis are usually seen in the
distal interphalangeal joints of the hand and the first carpometacarpal joint and
scaphotrapezial joint of the wrist. The PIP joints may occasionally be affected in
osteoarthritis. RA tends to involve the PIP and metacarpophalangeal joints of the
hand and all of the major joint compartments of the wrist (pancarpal
involvement). CPPD deposition disease usually initially affects the radiocarpal
joint in the wrist but may also involve the metacarpophalangeal joints of the
hand. The patterns of common arthropathies in the hips and knees are less
specific (Figures 16.15 and 16.16) but occasionally helpful. Even after one has
memorized the classic patterns of joint involvement by various arthropathies, it
is common to see joint diseases outside these common locations. A frequent
explanation for this is that any joint in the body can be affected by secondary
osteoarthritis due to trauma, infection, or another arthropathy.
•
FIGURE 16.4 Chondrocalcinosis is seen in the triangular fibrocartilage (arrow).
•
FIGURE 16.5 Chondrocalcinosis in the fibrocartilage menisci (arrowheads) and the
hyaline articular cartilage of the knee.
•
FIGURE 16.6 Diagram of a diarthrodial joint, demonstrating the periarticular bare
areas (arrows).
•
FIGURE 16.7 Erosions (arrows) are noted in the periarticular areas of the
metatarsophalangeal and toe joints in this patient with rheumatoid arthritis.
•
FIGURE 16.8 Erosions (arrows) are noted at the articular margins of the tibia in this
patient with juvenile chronic arthritis.
•
FIGURE 16.9 A gouty erosion (arrow) is noted along the medial margin of the first
metatarsal head in this patient with gout—relative sparing of the articular cartilage is
also noted.
•
FIGURE 16.10 Fusiform soft-tissue swelling of the proximal interphalangeal joint in
the hand of a patient with rheumatoid arthritis.
•
FIGURE 16.11 Sausage digit soft-tissue swelling of the index finger in the hand of a
patient with psoriatic arthritis. For comparison, the middle finger is normal.
•
FIGURE 16.12 Lumpy-bumpy soft-tissue swelling in the hand of a patient with
tophaceous gout. Bony erosions are also present.
FIGURE 16.13 • Typical distribution of arthritis in the hands. CPPD, calcium
pyrophosphate dihydrate; OA, osteoarthritis; RA, rheumatoid arthritis.
FIGURE 16.14 • Typical distribution of arthritis in the wrists. CPPD, calcium

RULE 4: DEMOGRAPHICS
Until this point, our diagnostic short list from the Sutton law includes
degenerative, depositional, and inflammatory arthropathies. However, this
differential diagnosis assumes that our patient is middle-aged or older. If arthritis
begins while a patient is young or if the arthritis is advanced in early adulthood,
we must consider a much different list of disorders (Table 16.5). Gender is also
occasionally helpful in refining the differential diagnosis of the arthropathies.
CPPD arthropathy affects both genders equally. RA has a moderate female
predominance, as does osteoarthritis in the older age group. Gout, on the other
hand, has a moderate to strong male predominance. Ankylosing spondylitis and
reactive arthritis have a very strong male predominance. Other demographic
factors, such as home location, occupation, and even ethnic subtype, can
occasionally be helpful in steering the differential toward or away from certain
disease entities.
FIGURE 16.15 • Typical distribution of arthritis in the knees. CPPD, calcium
FIGURE 16.16 • Typical distribution of arthritis in the hips. CPPD, calcium

RULE 5: OCCAM’S RAZOR VERSUS HICKAM’S DICTUM

Frustra fit per plura quod potest fieri per pauciora. (It is futile to do with more
things that which can be done with fewer.) This pronouncement is sometimes
known as Occam’s razor or as the law of parsimony. Yet another way of stating
it is “the simplest explanation is the best.” This maxim is often used in training
medical students, who are asked to ingest a patient’s history, physical
examination, laboratory results, and imaging findings and then regurgitate 1
diagnosis that explains everything. This rule works well enough until one starts
seeing real patients who have multiple simultaneous disorders. For those of you
who have rotated through a county or Veterans Affairs (VA) hospital, it is hard to
imagine a problem list with only 1 medical diagnosis listed. A more practical
rule for actual patients is Hickam’s dictum, commonly stated as: Patients can
have as many diseases as they damn well please. In regard to the diagnosis of
arthritis, we can further restate this as: Patients can have as many arthropathies
as they damn well please. The law of parsimony must frequently yield to
Hickam’s dictum when it comes to dealing with real patients. In the workup of
arthritis, this means that one occasionally notes findings that point in several
contradictory diagnostic directions. It is theoretically possible to see almost any
combination of arthropathies in a particular joint. For example, a single wrist
image might show chondrocalcinosis, erosions, osteophytes, and bony ankylosis
—findings pointing toward 4 potentially different arthropathies. The presence of
such apparently contradictory findings should be a strong hint to us that the law
of parsimony no longer applies. Exotic combinations of arthropathies, such as
gout and CPPD, gout and RA, RA and diffuse idiopathic skeletal hyperostosis,
RA and lupus (rhupus), exist but are, fortunately, uncommon. By far the most
common combination is osteoarthritis secondary to some other arthropathy.
Virtually any arthropathy that causes cartilage loss can lead to secondary
osteoarthritis, with all of the classic signs of osteoarthritis, including
osteophytes. In fact, in certain patients, the findings of the primary arthropathy
may be significantly obscured by the findings of secondary osteoarthritis.
Distinguishing primary from secondary osteoarthritis can be quite challenging.
In such cases, I find it helpful to look for concordance among the available
findings. In a primary arthropathy, the various findings are usually concordant.
Thus, in primary osteoarthritis, marked joint space narrowing is usually
accompanied by moderate or marked osteophytes. Discordance among these
findings is an important clue to diagnose if one may be dealing with secondary
osteoarthritis. For example, one might see fairly minimal osteophytes in the
presence of marked joint space narrowing or subchondral sclerosis. In fact, a
fairly common presentation of large joint RA (eg, knee or hip) is marked joint
space narrowing and subchondral sclerosis, with no evident erosions, and only
minimal osteophytes.
Table 16.5 ARTHROPATHIES OF YOUNGER PATIENTS
Juvenile idiopathic arthritis

Hemophilic arthropathy
Septic arthritis
Secondary osteoarthritis
A FINAL WORD
The 5 rules listed above are designed to quickly and ruthlessly lead one to a
diagnosis in most cases of arthritis. They are neither absolute nor
comprehensive, and they should not be followed dogmatically. Relying solely on
them for the diagnosis of arthritis is a bit like running one’s entire business based
solely on the maxim: “buy low, sell high.” Maxims become maxims because
they usually contain a concentrated dose of truth about a situation. However,
concentrating truth to this degree perforce requires leaving out a lot of important
and practical details.
References
1. Arthritis Foundation. Arthritis A to Z. http://www.arthritis.org/conditions-treatments/disease-center/.
2. Federal Bureau of Investigation. Willie Sutton. https://www.fbi.gov/history/famous-cases/willie-sutton.
Accessed February 05, 2012.
3. Braun HJ, Gold GE. Diagnosis of osteoarthritis: imaging. Bone. 2012;51(2):278–288.
doi:10.1016/j.bone.2011.11.019.
4. Jacobson JA, Girish G, Jiang Y, Sabb BJ. Radiographic evaluation of arthritis: degenerative joint disease
and variations. Radiology. 2008;248(3):737–747. doi:10.1148/radiol.2483062112.
5. Resnick D. Osteophytes, syndesmophytes, and other “phytes”. Postgr Rad. 1981;1:217–222.
6. Resnick D, Niwayama G. Entheses and enthesopathy. Anatomical, pathological, and radiological
correlation. Radiology. 1983;146:1–9.
7. Resnick D, Niwayama G, Goergen TG, et al. Clinical, radiographic and pathologic abnormalities in
calcium pyrophosphate dihydrate deposition disease (CPPD): pseudogout. Radiology. 1977;122(1):1–
15.
8. Resnik CS, Resnick D. Crystal deposition disease. Semin Arthritis Rheum. 1983;12(4):390–403.
9. Steinbach LS, Resnick D. Calcium pyrophosphate dihydrate crystal deposition disease revisited.
Radiology. 1996;200(1):1–9.
10. Jacobson JA, Girish G, Jiang Y, Resnick D. Radiographic evaluation of arthritis: inflammatory
conditions. Radiology. 2008;248(2):378–389. doi:10.1148/radiol.2482062110.
11. Tan YK, Conaghan PG. Imaging in rheumatoid arthritis. Best Pract Res Clin Rheumatol.
2011;25(4):569–584. doi:10.1016/j.berh.2011.10.002.
12. Harris MD, Siegel LB, Alloway JA. Gout and hyperuricemia. Am Fam Physician. 1999;59(4):925–934.
13. Monu JUV, Pope TL. Gout: a clinical and radiologic review. Radiol Clin N Am. 2004;42(1):169–184.
doi:10.1016/S0033–8389(03)00158–1.
14. Resnick D, Kransdorf MJ. Bone and Joint Imaging. 3rd ed. Saunders; 2004.
1. Sausage digit soft-tissue swelling in the hands is most closely associated with
which type of arthritis?
A. Rheumatoid arthritis
B. Osteoarthritis
C. Psoriatic arthritis
D. Gouty arthritis
2. Chondrocalcinosis is most closely associated with which type of arthritis?
A. Gouty arthritis
B. Rheumatoid arthritis
C. Osteoarthritis
D. Pyrophosphate arthropathy
3. Periostitis is most closely associated with which condition?

A. Spondyloarthropathy
C. Osteoarthritis
D. Tophaceous gout
4. Which radiographic feature is most closely associated with inflammatory types

of arthritis?
A. Osteophytes
B. Erosions
C. Joint space narrowing
D. Subluxation

1. C Psoriatic arthritis is associated with sausage digit soft-tissue swelling.
2. D Chondrocalcinosis is associated with pyrophosphate arthropathy, but not
the other options.
3. A Periostitis is associated with spondyloarthropathy, but not the other
options.
4. B Erosions are the hallmark of inflammatory arthritis.
17
Imaging of Osteoarthritis
This chapter discusses the radiology of the most prevalent form of arthritis.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of osteoarthritis, the learner will be
able to
4. summarize relevant concepts and knowledge for the following topics: primary osteoarthritis;
cartilage, bone, and soft-tissue abnormalities in osteoarthritis; osteoarthritis in the knee, hip,
shoulder, and spine; secondary osteoarthritis; inflammatory osteoarthritis; intervertebral disk
degeneration; diffuse idiopathic skeletal hyperostosis (DISH); and Baastrup disease.
PRIMARY OSTEOARTHRITIS
Osteoarthritis is a form of joint disease characterized by degenerative changes in
the bone and cartilage of synovial joints. Osteoarthritis can be divided into
primary and secondary types, but the division is artificial: The underlying cause
is evident in secondary osteoarthritis but not in primary or idiopathic
osteoarthritis. The distinction has some practical value in understanding the
process and planning clinical management.
As mentioned earlier, osteoarthritis is the most common form of arthritis. Its
prevalence increases with age, so that osteoarthritis is nearly ubiquitous in
patients older than 65 years. Up to 45 years of age, it is more prevalent in men;
from 45 to 55 years, the prevalence is equal; and after 55 years, it is more
prevalent in women. The most common presentation of osteoarthritis is joint
pain and limitation of activity. There are no specific laboratory tests for
osteoarthritis; rather, any tests performed are usually used to eliminate other
forms of arthritis as clinical possibilities.
ANATOMY AND PHYSIOLOGY OF ARTICULAR CARTILAGE

The ends of the articulating bones (ie, the joint surfaces) are covered with
hyaline articular cartilage. Hyaline cartilage is composed of a collagen fibril
framework and a ground substance. One set of densely packed collagen fibrils is
oriented parallel to the articular surface, forming an armor-plate layer with tiny
surface pores that allow the passage of water and small electrolytes. A second,
less densely packed set of collagen fibrils is oriented in arcades, linking the
armor-plate layer to the subchondral bone (Figure 17.1).
The ground substance is a gel that consists of water and large proteoglycan
aggregate macromolecules that are loosely fixed to the collagen framework. The
proteoglycan macromolecules are too large to pass through the pores of the
armor-plate layer. The physical and chemical properties of these macromolecules
allow them to attract and bind water, providing sufficient swelling pressure
beneath the armor-plate layer to inflate the articular cartilage, even during
weight bearing. During motion, a thin layer of water is expressed through the
small surface pores, providing a frictionless surface for a lifetime of mobility.
Articular cartilage has a load-dampening ability that spreads transmitted loads
over a greater area of the subchondral bone. Under rapid, transient loading,
articular cartilage has elastic properties. Under a steady load, it creeps and
deforms like a sponge. The portion of cartilage that is adjacent to the
subchondral bone is calcified.
Interdigitations between the calcified cartilage and the subchondral bone
provide a strong mechanical coupling. Chondrocytes are the cells whose
metabolic activity maintains the specialized structures of articular cartilage. Less
than 1% of articular cartilage volume is composed of cells. Because cartilage is
avascular and alymphatic, chondrocytes derive their nutrients by passive
diffusion from the synovial fluid. This passive diffusion is amplified by an active
pumping action that occurs as joint fluid is forced in and out of the cartilage
during loading and unloading. Because of this avascularity, articular cartilage
has only a limited ability to repair itself. Deep injuries may repair with cartilage
that is densely fibrous.
•
FIGURE 17.1 Structure of articular cartilage.
CARTILAGE ABNORMALITIES IN PRIMARY

OSTEOARTHRITIS
The early morphologic abnormality in primary osteoarthritis is fibrillation of the
articular cartilage. The surface develops fibril-like projections and becomes
irregular. Underlying this morphologic change is disruption at the molecular
level of the superficial armor-plate layer and collagen framework, resulting in
progressive loss of proteoglycans from the ground substance and collagen from
the framework. Chondrocytes increase protein synthesis, presumably in response
to the continuing loss of structural components. Progressive erosion and
formation of fissures in the surface eventually expose the subchondral bone. The
initial event that incites fibrillation of the cartilage surface is unknown; some
forms of primary osteoarthritis may result from an initial alteration in articular
cartilage physiology.
Cartilage abnormalities are inferred from the radiolucent gap between
articulating bones, which is called the articular space or joint space. The articular
cartilage fills most of this space, with a small potential space located between the
articulating surfaces. Loss of articular cartilage causes the joint space to narrow.
Other than this, radiographic findings do not appear in osteoarthritis until
articular cartilage loss results in secondary adaptive changes in bone.
BONE ABNORMALITIES IN PRIMARY OSTEOARTHRITIS

Bone findings in osteoarthritis include uneven subchondral sclerosis,
osteophytes, and subchondral cysts; the absence of osteoporosis, ankylosis, and
erosions is characteristic. Sclerosis, also called eburnation, is new bone apposed
to the trabeculae of existing bone, usually in a subchondral location
(immediately beneath the articular cartilage) but sometimes on the surface after
the cartilage is gone (Figure 17.2).
Subchondral cysts (also called geodes) occur when cracks or fissures in the
articular surface allow the intrusion of synovial fluid into the subchondral
cancellous bone (Figure 17.3). However, subchondral cysts are seen in virtually
all types of arthritis and have no particular differential diagnostic significance.
Osteophytes occur in the presence of cartilage loss and represent new
excrescences of cartilage and bone that enlarge the articular surface at its
margins. Osteophytes tend to be the largest in the plane of motion; therefore,
osteophytes at the distal interphalangeal (DIP) and proximal interphalangeal
(PIP) joints are best seen on the lateral view. In the hand and wrist, primary
osteoarthritis typically affects the DIP and PIP joints and the basal joints of the
thumb (Figure 17.4).
FIGURE 17.2 • Marked osteoarthritis of the hand and wrist with prominent
osteophytes, joint space narrowing, and subchondral sclerosis in the distal
interphalangeal, proximal interphalangeal, first carpometacarpal, and scaphotrapezial
joints. The subchondral sclerosis is particularly marked in the scaphotrapezial joint.
Faint chondrocalcinosis is noted in the triangular fibrocartilage complex.
FIGURE 17.3 • Moderate glenohumeral osteoarthritis of the shoulder with an
osteophyte and several subchondral cysts in the humeral head (arrows).
•
FIGURE 17.4 Degenerative joint disease at the first carpometacarpal joint with
narrowing of the articular space, osteophyte formation, subchondral sclerosis, and
subluxation.
•
FIGURE 17.5 Moderate femorotibial osteoarthritis with marginal osteophytes.
The basal joints of the thumb are composed of the first carpometacarpal joint
and the scaphoid-trapezium-trapezoid joints. Isolated degenerative involvement
at this specific site is virtually diagnostic of primary osteoarthritis. The first
metatarsophalangeal joint, hips and knees, and the cervical and lumbar spine are
also common sites of involvement. The metacarpophalangeal joints, wrist,
elbow, shoulder, and ankle are typically spared. The severity of radiographic
findings does not necessarily correlate with the severity of symptoms.
KNEE OSTEOARTHRITIS
In the knee, the characteristic distribution of involvement is in the medial
compartment and, to a less severe degree, the patellofemoral compartment. Joint
space narrowing, subchondral sclerosis, osteophytes, and subchondral cysts are
typical findings (Figure 17.5). Occasionally, more severe involvement of the
lateral or patellofemoral compartments occurs (Figure 17.6).
Angular deformities and joint space narrowing are best demonstrated on
standing views. Because the severity of involvement of the anterior and posterior
portions of the femoral cartilage is typically uneven, the amount of joint space
narrowing may vary between radiographs with the knee in extension and flexion.
On MRI, early osteoarthritis is evident as an abnormal high signal in articular
cartilage on T2 MRI (Figures 17.7 and 17.8). When isolated to the patella, this
condition is called chondromalacia patellae. Fibrillation of the cartilage surface,
thinning of the cartilage, and frank loss of cartilage may be seen in progressively
more severe cases. Subchondral bone edema at sites of cartilage loss, osteophyte
formation, intra-articular bodies, and effusions may be present in established
osteoarthritis (Figures 17.9 and 17.10).
HIP OSTEOARTHRITIS
In the hip, loss of articular space is usually found along the superior (horizontal)
portion of the joint. Less commonly, the medial joint space is narrowed (Figures
17.11 and 17.12). Osteophyte formation in the femoral head often forms a collar
of bone around the femoral neck at the margin of the articular surface, usually
seen best on frog lateral views. As with the knee, uneven involvement of the
articular cartilage results in varying amounts of joint space narrowing from
position to position. Mapping cartilage thickness with fluoroscopically
positioned spot radiographs or cartilage-specific imaging parameters on MRI can
be helpful in planning rotational osteotomies for treatment.
Idiopathic rapidly destructive osteoarthritis of the hip is a severe form of
arthritis that typically affects older women. Radiographs show severe joint space
loss and some of the typical features of osteoarthritis, but the condition
progresses rapidly, sometimes resulting in subchondral collapse and complete
destruction of the joint in less than a year.1
SHOULDER OSTEOARTHRITIS
Osteoarthritis of the acromioclavicular and glenohumeral joints is a common
finding on shoulder imaging. On radiographs, osteophytes may be seen (Figure
17.13). On MRI, osteophytes and hypertrophy of these joints are typical, often
with subchondral edema and fluid in the joints (Figure 17.14).
Rotator cuff arthropathy is a distinct form of glenohumeral arthropathy in
which there is a massive rotator cuff tear that leads to superior subluxation of the
humeral head, remodeling of the undersurface of the acromion, and abnormal
shoulder function.
•
FIGURE 17.6 Marked patellofemoral osteoarthritis with asymmetric joint space loss
and osteophyte formation at the lateral facet.
•
FIGURE 17.7 Axial PD FS MRI of a knee with chondromalacia patella. Asymmetric
narrowing of the medial patellar cartilage is noted, with increased signal intensity in
the remaining cartilage (arrow) and focal adjacent marrow edema. Incidentally noted
is marked susceptibility artifact in the distal femur from a prior anterior cruciate
ligament repair.
SPINE OSTEOARTHRITIS
There are many synovial joints in the axial skeleton. These include the facet
joints of the spine, the atlantoaxial (C1-C2) joint, the uncovertebral joints of the
cervical spine, and the lower two-thirds of the sacroiliac joints. Osteoarthritis of
the synovial joints of the spine may be the predominant feature of degenerative
spine disease or may occur in association with other features such as
degenerative disk disease, previous trauma, scoliosis, kyphosis, or vertebral
anomalies. The common sites of synovial joint osteoarthritis are the lower
cervical and lower lumbar spine. The atlantoaxial joint is also synovial and may
be affected. The pathologic process is identical to that of other synovial joints,
leading to joint space narrowing, subchondral sclerosis, and osteophytes. Loss of
articular cartilage may allow subluxation or excessive motion; bony hypertrophy
may reduce motion. Osteophytes and ligamentous thickening may lead to nerve
root involvement. These findings are best demonstrated by CT (Figure 17.15).
•
FIGURE 17.8 Axial PD FS MRI of the knee shows chondromalacia patella, with
fissuring in the patellar cartilage. Focal marrow edema is noted adjacent to the larger
fissure.
SECONDARY OSTEOARTHRITIS
Secondary degenerative changes in the joints result from 3 major factors: an
abnormality of the articular cartilage, loss of subchondral bony support beneath
normal articular cartilage, and abnormal alignment and mechanical stress. Any
condition with one of these features may lead to permanent, progressive
osteoarthritis. Secondary osteoarthritis may follow inflammatory arthritis if the
inflammatory process has caused permanent cartilage damage and is quiescent
long enough for the degenerative changes to develop. Mechanical trauma may
injure the articular cartilage, which has a limited ability for repair. A
fibrocartilage scar may replace damaged areas of hyaline cartilage. Joint debris,
intra-articular bodies, or displaced meniscal fragments within a joint may erode
the articular cartilage. Osteochondral intra-articular bodies derive nutrition from
synovial fluid and may grow. Healthy cartilage wears prematurely when its
underlying bony support is lost. For example, collapse of the subchondral bone
of the femoral head after osteonecrosis leads rapidly to secondary degeneration.
Less obvious changes in the subchondral bone due to repetitive subclinical
trauma may also lead to osteoarthritis. An abnormally aligned joint or a joint that
is subject to mechanical disadvantage, instability, or abnormal stresses may wear
prematurely. However, posttraumatic osteoarthritis may occur even with ideal
fracture treatment2; this phenomenon probably reflects irreparable cartilage
injury at the time of trauma (Figure 17.16).
Many forms of developmental and acquired bone and joint dysplasia lead to
early osteoarthritis, including developmental dysplasia of the hip (Figure 17.17),
Legg-Calvé-Perthes disease (Figure 17.18), and multiple epiphyseal dysplasia.
The premature wear resulting from the abnormal joint geometry worsens in a
vicious cycle of progressive malalignment, mechanical disadvantage, and
abnormal stress.
•
FIGURE 17.9 Osteoarthritis. A, Coronal T1 MRI shows cartilage loss and meniscal
extrusion (arrow) in the medial compartment. Medial and lateral compartments are
involved by osteophytes. B, Sagittal T2 FS MRI shows patellofemoral compartment
osteophytes (arrow) and cartilage loss. C, Sagittal T2 FS MRI through the medial
compartment shows effusion, cartilage loss, osteophytes, and degenerative posterior
horn medial meniscal tear (arrow).
INFLAMMATORY (EROSIVE) OSTEOARTHRITIS OF THE

HAND
Inflammatory (erosive) osteoarthritis is a condition in which acute synovitis
accompanies primary osteoarthritis.3 Although joint degeneration always has
some component of synovial inflammation because of the presence of joint
debris and cartilage breakdown products, the inflammation dominates the
clinical presentation in erosive osteoarthritis. Radiographs show the degenerative
features and distribution of primary osteoarthritis, but the acute synovitis causes
inflammatory erosions, uniform joint space narrowing, and sometimes ankylosis.
A characteristic “seagull” appearance may be seen on posteroanterior
radiographs at the interphalangeal joints of the fingers, corresponding to central
erosions and bony hypertrophy (Figure 17.19). The typical age at onset is in the
fifth or sixth decade, and women are affected far more frequently than men. The
inflammation usually subsides within a few months to a couple of years, leaving
the degenerative changes. In the hand, erosive osteoarthritis characteristically
affects the DIP and PIP joints and the basal joints of the thumb, as does
nonerosive primary osteoarthritis.
DEGENERATIVE SPINE CONDITIONS

Disk Degeneration
Besides the synovial facet joints, there are also a number of nonsynovial joints in
the spine, known as the intervertebral disk joints. These joints are present along
the anterior portion of the spine. An intervertebral disk joint comprises
cartilaginous end plates covering the articulating surfaces of adjacent vertebral
bodies, a central nucleus pulposus, and a circumferential annulus fibrosus
(Figure 17.20).
•
FIGURE 17.10 Marked patellofemoral osteoarthritis with several large, calcified
intra-articular bodies posterior to the knee joint within a popliteal cyst.
•
FIGURE 17.11 Marked osteoarthritis of the hip with prominent osteophytes, marked
joint space narrowing, acetabular protrusion, and a large subchondral cyst in the
superior acetabulum. Joint space narrowing is present both superiorly and medially,
resulting in axial migration of the femoral head.
•
FIGURE 17.12 Osteoarthritis of the hip with advanced joint space asymmetric
narrowing and prominent osteophytes on coronal CT.
FIGURE 17.13 • Moderate glenohumeral osteoarthritis of the shoulder with
osteophyte formation inferiorly and several large intra-articular bodies in the
subcoracoid recess (arrows).
In the child, the nucleus pulposus has a gelatinous character; in the adult, the
nucleus pulposus has converted to fibrocartilage. The annulus fibrosus contains
an outer zone of collagenous fibers and an inner zone of fibrocartilage. The
annulus fibrosus is anchored to the cartilaginous end plates, the vertebral rim,
and the periosteum of the vertebral body. The anterior longitudinal ligament is
applied to the anterior aspect of the vertebral column with firm attachments to
the periosteum near the corners of the vertebral bodies. A posterior longitudinal
ligament is applied to the posterior aspect of the vertebral bodies. This same
structure and physiology are found at the symphysis pubis.
•
FIGURE 17.14 Moderate glenohumeral osteoarthritis of the right shoulder. A, Axial
PD FS MRI shows the hyaline articular cartilage is thinned and irregular and a
subchondral cyst is noted in the anterior portion of the humeral head (arrow). B,
Coronal PD FS MRI shows thinning and irregularity of the hyaline articular cartilage
with an osteophyte on the inferior margin of humeral head (solid white arrow). A
subchondral cyst is noted in the superior portion of the humeral head (open black
arrow). C, Sagittal PD FS MRI shows high signal in the acromioclavicular (AC) joint
(arrow), consistent with AC osteoarthritis.
The intervertebral disk spaces should be proportional to the width of the

vertebral body. They are relatively small in the cervical region but gradually
become thicker in the thoracic and lumbar regions. Narrowing is characteristic of
degenerative disk disease, and calcification or gas in the disk space is
pathognomonic. Degeneration of the nucleus pulposus, the annulus fibrosus, or
both may be present.4,5 Although these processes can often be distinguished
from each other, an overlap in findings will be seen in many patients who have
both processes occurring in the same disk (Figures 17.21–17.23). The key
distinguishing characteristic between these 2 processes is disk space narrowing.
If present, this is strongly suggestive of degenerative nuclear disease. This is
often accompanied by endplate sclerosis and mild to moderate osteophytosis.
Degenerative annular disease is not always associated with significant disk
space narrowing, and the marginal osteophytes seen with this entity, sometimes
referred to as spondylosis deformans, are often much larger than those seen with
degenerative nuclear disease. In practice, one often sees evidence of
degeneration of both the annulus and the nucleus. It usually does not make a lot
of difference to the referring clinician which component of the disk has
degenerated. Therefore, I suggest using the term “disk degeneration” in one’s
dictations to refer to both of these entities. Disk degeneration may lead to
abnormalities of alignment, including intervertebral subluxation, exaggerated
kyphosis or lordosis, kyphosis or lordosis at inappropriate levels, and scoliosis.
Images of the patient in flexion, extension, or lateral bending may be required to
demonstrate abnormal mobility or loss of mobility.
Most of the phytes seen in the spine are due to disk degeneration. However,
bony excrescences can form along the margins of the disk spaces secondary to
inflammation. This can be seen in a number of spondyloarthropathies, such as
ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and arthritis
associated with inflammatory bowel disease. These syndesmophytes tend to be
oriented fairly vertically (Figure 17.24), as opposed to the more horizontally
oriented or bowed appearance of the osteophytes seen with disk degeneration.
However, in practice, it can sometimes be difficult to distinguish these 2 types of
phytes.
•
FIGURE 17.15 Axial CT of the lumbar spine, demonstrating marked bilateral facet
joint osteoarthritis.
Diffuse Idiopathic Skeletal Hyperostosis

DISH (ankylosing hyperostosis of the spine, Forestier disease) is an idiopathic
disorder, characterized by ossification of the soft tissues at the attachments of
muscles, ligaments, and tendons to bone. DISH appears to represent an ossifying
diathesis or bone-forming tendency of unknown etiology that increases in
incidence with age. DISH is common in older adults, more frequently men, and
the symptoms are often back stiffness and pain. In DISH, flowing ossification,
usually along the anterior longitudinal ligament, is seen.6 DISH is a diagnosis of
exclusion and should be distinguished from spondylosis deformans,
intervertebral osteochondrosis, and ankylosing spondylitis.7 Extraspinal
manifestations of DISH are exceedingly common in older patients. Ossification
at the insertion of tendons may be seen throughout the extremities. In the pelvis,
whiskering bone proliferation is common along sites where muscles and
ligaments attach. Para-articular bone growths correspond to ossification at the
attachments of joint capsules. Extra-articular bony ankylosis is very common in
the thoracic spine and somewhat less common in the cervical and lumbar regions
(Figures 17.25 and 17.26). Extra-articular ankylosis of the spine makes the spine
stiff. Despite the increase in bone mass, the spine is more fragile
biomechanically when subjected to trauma. The lack of motion and the loss of
the energy-absorbing function of the intervertebral disks and ligaments
contribute to its decreased ability to absorb loading. Fractures and fracture-
dislocations of the spine may be catastrophic (Figure 17.27). For practical
purposes, the diagnosis of DISH can be made radiographically when there is
excessive entheseal ossification in the absence of other conditions known to
cause such ossification.
•
FIGURE 17.16 Posttraumatic ankle osteoarthritis. A, Postsurgical appearance
following open reduction and internal fixation of trimalleolar ankle fracture, at the age
of 27 years. Note the normal thickness of the tibiotalar cartilage spaces. B and C,
Coronal and sagittal CT show marked cartilage loss from the tibiotalar articular
surfaces with subchondral cysts and subchondral sclerosis, at the age of 35 years.
•
FIGURE 17.17 Developmental dysplasia of the hip joint with chronic dislocation,
pseudoacetabulum formation, and marked secondary osteoarthritis.
•
FIGURE 17.18 Right hip joint in a patient with Legg-Calvé-Perthes disease as a
child and marked secondary osteoarthritis.
•
FIGURE 17.19 Hand radiograph of a 69-year-old man with erosive osteoarthritis
involving the distal interphalangeal (DIP), proximal interphalangeal, and first
carpometacarpal joints. Note the gull-wing pattern in the DIP joints.
•
FIGURE 17.20 Anatomy of an intervertebral disk joint.
•
FIGURE 17.21 Triangular osteophytes (arrows) of spondylosis deformans with
degenerative disk changes. The disk spaces are narrowed and the subchondral bone
is sclerotic.
•
FIGURE 17.22 Lumbar degenerative disk disease. A and B, Coronal and sagittal
CT show marked intervertebral disk space narrowing, intradiscal gas, endplate
sclerosis, and osteophytosis at L4-L5 and L5-S1.
•
FIGURE 17.23 Degenerative lumbar disk herniation. Sagittal T2 MRI shows
degenerative disk disease (low signal) at L4-L5 and L5-S1. The L4-L5 disk has
herniated posteriorly (long arrow). Note normal disk height and normal hydration (high
signal) of the nucleus pulposus at L3-L4 and L2-L3 (short arrows).
•
FIGURE 17.24 Lateral radiograph of the lumbar spine in a patient with ankylosing
spondylitis and multiple vertically oriented syndesmophytes (arrow).
•
FIGURE 17.25 Prominent, flowing ossification is noted along the anterior margin of
the cervical spine in this patient with diffuse idiopathic skeletal hyperostosis.
Considering that the esophagus is located immediately anterior to the cervical spine,
it is easy to see why such patients often complain of dysphagia.
FIGURE 17.26 • Diffuse idiopathic skeletal hyperostosis with diffuse, flowing
ossification (arrows) of the paravertebral soft tissues. A, Sagittal CT shows the
ossification (arrows) extending over multiple contiguous levels. B, Axial CT shows the
ossification (arrow) is asymmetric.
•
FIGURE 17.27 Fracture through diffuse idiopathic skeletal hyperostosis (DISH). 82-
year-old man with DISH who was injured in a ground level fall. Sagittal CT of the
midthoracic spine, right (A), midline (B), left (C), shows extensive flowing ossification
of the anterior longitudinal ligament from DISH that bridges multiple intervertebral
levels. There is a fracture through the ossification on the right (arrows) that continues
through the T7 vertebral body and exits posteriorly through the T7-T8 disk
(arrowhead).
•
FIGURE 17.28 Baastrup disease (different patients). A, Lateral radiograph shows
hyperostosis of the spinous processes with kissing spines (arrow). B, Sagittal CT
shows kissing spines (arrow).
Baastrup Disease
Baastrup disease (osteoarthrosis interspinalis) is a degenerative condition
described in the lumbar spine in which there is hyperostosis of the spinous
processes leading to remodeling and joint formation between adjacent spinous
processes (Figure 17.28). The condition has also been described as kissing
spines, referring to the remodeling of adjacent spinous processes. The
relationship of Baastrup disease to chronic low back pain is uncertain, and both
are common.8
References
1. Porrino J, Carlson B, Kani KK, Mulcahy H, Wyatt A, Chew FS. Disappearing acts: the many causes of
rapidly destructive arthritis. Curr Probl Diagn Radiol. 2017;46(1):63–73. doi:10.1067/j.
cpradiol.2016.02.012 [Epub February 27, 2016. PMID:27020254].
2. Horisberger M, Valderrabano V, Hintermann B. Posttraumatic ankle osteoarthritis after ankle-related
fractures. J Orthop Trauma. 2009;23(1):60–67. doi:10.1097/BOT.0b013e31818915d9
[PMID:19104305].
3. Punzi L, Frigato M, Frallonardo P, Ramonda R. Inflammatory osteoarthritis of the hand. Best Pract Res
Clin Rheumatol. 2010;24(3):301–312. doi:10.1016/j.berh.2009.12.007 [PMID:20534365].
4. Resnick D. Degenerative diseases of the vertebral column. Radiology. 1985;156(1):3–14.
5. Resnick D. Osteophytes, syndesmophytes, and other “phytes.” Postgraduate Rad. 1981;1:217–222.
6. Taljanovic MS, Hunter TB, Wisneski RJ, et al. Imaging characteristics of diffuse idiopathic skeletal
hyperostosis with an emphasis on acute spinal fractures: self-assessment module. AJR Am J Roentgenol.
2009;193(3 suppl):20–24. doi:10.2214/AJR.09.7169.
7. Resnick D, Niwayama G. Radiographic and pathologic features of spinal involvement in diffuse
idiopathic skeletal hyperostosis (DISH). Radiology. 1976;119(3):559–568.
8. Alonso F, Bryant E, Iwanaga J, Chapman JR, Oskouian RJ, Tubbs RS. Baastrup’s disease: a
comprehensive review of the extant literature. World Neurosurg. 2017;101:331–334.
doi:10.1016/j.wneu.2017.02.004 [Epub February 10, 2017. PMID:28192272].
1. Which radiographic feature is most characteristic of rheumatoid arthritis?

A. Osteoporosis
B. Subchondral cysts
C. Ankylosis
D. Eburnation
2. Which of the following radiographic features is typically not found in

rheumatoid arthritis?
A. Subchondral cysts
B. Joint space narrowing
C. Soft-tissue swelling
D. Chondrocalcinosis
3. Radiographic involvement of which of the following joints is most closely

associated with rheumatoid arthritis?
A. DIP joints of the fingers
B. First carpometacarpal joint
C. Lesser metatarsophalangeal joints
D. Symphysis pubis
4. Which radiographic finding in the hand and wrist distinguishes rheumatoid

arthritis from psoriatic arthritis?
A. Osteophytes
B. Periostitis
C. Erosions
D. Subchondral cysts

1. A Osteoporosis is a characteristic feature of rheumatoid arthritis.
Subchondral cysts may occur but are nonspecific and more commonly found in
osteoarthritis.
2. D Chondrocalcinosis does not occur in rheumatoid arthritis.
3. C The lesser metatarsophalangeal joints of the foot are the most commonly
affected sites among the options listed.
4. B Periostitis is found in psoriatic arthritis but generally not in rheumatoid
arthritis. Osteophytes are generally not found in either, and erosions and
subchondral cysts may be found in both.
18
Imaging of Inflammatory Arthritis
This chapter covers the clinical forms of arthritis and connective tissue disease
that present on radiographs with a preponderance of inflammatory changes.
Septic arthritis is covered in the chapter on musculoskeletal infections.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of inflammatory arthritis, the learner
will be able to
4. summarize relevant concepts and knowledge for the following topics: rheumatoid arthritis,
including pathologic-radiologic features and extra-articular manifestations; connective tissue
diseases, including systemic lupus erythematosus (SLE), scleroderma, dermatomyositis, and
polymyositis; spondyloarthropathy, including ankylosing spondylitis, reactive arthritis, psoriatic
arthritis, and enteropathic spondyloarthropathy; and juvenile idiopathic arthritis in adults.
RHEUMATOID ARTHRITIS
Rheumatoid arthritis is a systemic autoimmune disease manifested in the
musculoskeletal system by inflammatory polyarthritis of the synovial joints.1
The pathogenesis is not understood, and no causative agent has been proved.
Genetic factors affect susceptibility to and expression of the disease. Rheumatoid
arthritis is usually distinguished from other arthritides by the presence of
rheumatoid factor (RF) in the serum. Rheumatoid arthritis has a prevalence of
1% in the general population, with women affected more often than men by a 3:1
ratio. High RF titers often correlate with more severe disease. The typical age
range of presentation is 25 to 55 years. In 70% of cases, the onset is insidious
and occurs over weeks to months; in 20%, the onset occurs over days to weeks;
and in 10%, the onset is acute and occurs over hours to days. The acute onset
mimics the onset of septic arthritis. The clinical course of rheumatoid arthritis is
progressive in 70% of cases, leading to disabling, destructive disease. The
clinical progression may be rapid or slow. In 20%, the disease is intermittent
with remissions generally lasting longer than exacerbations, and in 10%,
remissions last several years. The clinical diagnosis is based on criteria that
include morning stiffness; symmetric swelling of the proximal interphalangeal
(PIP), metacarpophalangeal (MCP), or wrist joints; rheumatoid nodules; serum
RF; and specific radiographic findings.
Pathologic-Radiologic Features
The underlying pathologic change in rheumatoid arthritis is chronic synovial
inflammation with hyperemia, edema, and production of excess fluid.2
Chronicity leads to hypertrophy and fibrosis. Hypertrophic, chronically inflamed
synovium is called pannus. Pannus dissolves the cartilage and bone by the
actions of enzymes along its advancing margin. Commonly seen early
radiographic findings include fusiform periarticular soft-tissue swelling—
corresponding to synovial hypertrophy and joint effusion—and acute erosions at
the margins of the joint. Articular cartilage may also be dissolved by enzymes
released into the joint space, causing uniform narrowing of the joint space on
radiographs. Synovial hyperemia causes juxta-articular osteoporosis. There is a
characteristic lack of reactive bone formation. Common late radiologic findings
include chronic generalized osteoporosis, progression of marginal erosions to
severe erosions involving subchondral bone, synovial cyst formation,
subluxations and abnormalities of alignment, and secondary osteoarthritis. Not
all findings are present at any one time in individual patients; observation of
combinations of these findings should lead to the correct diagnosis. The
distinctive radiographic pattern of chronic osteoporosis, marginal erosions, and
little if any reactive bone formation is the hallmark of rheumatoid arthritis.
Although the appendicular skeleton tends to be extensively involved, the axial
skeleton is usually spared except for the upper cervical spine. Bilaterally,
symmetric clinical involvement is usual, but the severity of radiologic
involvement is not necessarily symmetric, especially when radiographs are
obtained early in the clinical course. Secondary degenerative changes may occur
if the inflammatory process remits for several years. Both rheumatoid arthritis
and primary osteoarthritis are common conditions; patients with both diseases
may have confusing radiographic findings.
Sonography and MRI are more sensitive than radiography in detecting
synovitis,3,4 the primary abnormality in rheumatoid arthritis. Subchondral bone
marrow edema may occur with synovitis, and both are precursors of bone
erosions. Erosions will not occur in the absence of synovitis. MRI criteria for
diagnosing rheumatoid arthritis include periarticular contrast enhancement of the
wrist or the MCP or PIP joints in both hands, marrow edema, erosions, joint
effusion, synovial sheath effusion, and cartilage irregularity and thinning.
Gadolinium helps distinguish nonenhancing joint fluid from enhancing synovial
proliferation and pannus. Successful treatment of early rheumatoid arthritis with
disease-modifying antirheumatic drugs (DMARDs) that suppress synovitis may
be evident on MRI as the reversion of synovitis and marrow edema to normal.
MRI is also helpful in the evaluation of the complications of rheumatoid arthritis
at the craniocervical junction and elsewhere.
The treatment of rheumatoid arthritis is aimed for the control of synovitis and
the prevention of joint injury.1 Rheumatoid arthritis was associated with a high
degree of morbidity and early mortality before the widespread use of
methotrexate that began in the 1980s, more aggressive treatment of early
disease, and the availability of targeted biologic agents since the later part of the
1990s. Clinical outcomes have improved significantly with changes in drug
therapy and in the approach to treatment. Common principles that guide
management include approaches directed at achieving remission or low disease
activity by more rapid and sustained control of inflammation by the institution of
DMARD therapy early in the disease course. DMARDs, including nonbiologic
(traditional small molecule or synthetic) and biologic DMARDs, have the
potential to reduce or prevent joint damage and to preserve joint integrity and
function. The nonbiologic DMARDs most frequently used include
hydroxychloroquine, sulfasalazine, methotrexate, and leflunomide. Biologic
DMARDs, produced by recombinant DNA technology, generally target
cytokines or their receptors or are directed against other cell surface molecules.
FIGURE 18.1 • Rheumatoid hand of different patients. A, Juxta-articular
osteoporosis, soft-tissue swelling, and early erosive changes at the
metacarpophalangeal (MCP) (arrows) and first carpometacarpal (CMC) joints are
present. B, Juxta-articular osteoporosis is present. Small erosions and fusiform soft-
tissue swelling are present at the proximal interphalangeal joints of the middle and
ring fingers and the MCP joint of the index finger (arrow). Uniform joint space loss is
present throughout the carpus. There are erosions on both sides of the first CMC
joint.
FIGURE 18.2 • Rheumatoid metacarpophalangeal (MCP) erosions. A, Hand
radiograph shows soft-tissue swelling at the second MCP joint (arrow) and erosions at
the second metacarpal head. B, Sonogram of the second MCP joint shows erosions
of the metacarpal head filled with pannus (arrows). Courtesy Mitchell Kline, MD.
•
FIGURE 18.3 Rheumatoid arthritis involving the metacarpophalangeal joint of the
ring finger. A, Radiograph shows early subchondral bone erosion. Erosive changes
are manifested by loss of the white cortical line along the radial aspect of the fourth
metacarpal head (arrow). B, Coronal T2 FS MRI shows effusion (arrow). C, Coronal
T1 FS Gd MRI shows synovial enhancement (arrow).
Hand and Wrist
There is considerable variability in the distribution of radiographic abnormalities
in rheumatoid arthritis, and the findings on radiographs may not correlate with
the clinical features.2–5 The earliest radiographic changes are fusiform soft-tissue
swelling and juxta-articular osteoporosis (Figure 18.1). In the hand, rheumatoid
arthritis classically involves the MCP and PIP joints. The earliest bone erosions
are generally at the MCP joints (Figures 18.2 and 18.3), often the second and
third on the radial side. The PIP joint of the middle finger is another site of
typical early involvement. Oblique radiographs may show subtle subchondral
bone resorption. Fusiform soft-tissue swelling, juxta-articular osteoporosis,
concentric loss of cartilage space, and acute marginal erosions may be seen
(Figure 18.4). Compressive erosions and remodeling of bone may result from the
collapse of osteoporotic bone by muscle tension; this is especially common at
the MCP joints. Loss of the normal balanced tension at the digits results in
various alignment deformities, including the swan neck and boutonniere
deformities of the fingers and the Z-shaped deformity of the thumb (Figure
18.5). Superficial erosions of the cortex may occur beneath inflamed tendon
sheaths, especially along the outer aspect of the distal ulna, the dorsal aspect of
the first metacarpal, and the proximal phalanx of the first digit.
In the wrist, pancompartmental involvement is usual (Figure 18.6). The
earliest bone changes are erosions at the ulnar and radial styloid processes and
the waists of the capitate and scaphoid bones. On MRI, erosions are evident as
focal defects in the bone that are low to intermediate T1 signal and high T2
signal. The pannus within the erosions enhances with gadolinium (Figure 18.7).
Malalignment in advanced disease results from the loss of balanced muscular
tension and ligamentous restriction. Involvement of tendons can be demonstrated
by MRI (Figure 18.8) where the synovial sheaths show fluid and high T2 signal.
The inflamed synovium enhances with gadolinium.
Other Peripheral Joints

In the elbow, synovial hypertrophy and effusion provide a fat pad sign. As in
other joints, periarticular osteoporosis, uniform joint space narrowing, and
erosions are seen. In the glenohumeral joint, erosions are especially prominent
around the proximal humerus, and rotator cuff tear or atrophy causes superior
subluxation of the humeral head and adaptive changes in the inferior surface of
the acromion from the humeral head (Figures 18.9 and 18.10). Resorption of the
distal clavicle and widening of the acromioclavicular joint are frequently
observed in rheumatoid arthritis. In the knee, meniscal invasion by pannus
occurs early and may be detectable on MRI. The typical inflammatory changes
may be superimposed on secondary degenerative changes, but the proliferative
bone response is disproportionately modest in comparison to the loss of joint
space (Figure 18.11). On MRI, effusions, erosions, diffuse cartilage loss, bone
marrow edema, and pannus may be demonstrated at the knee (Figure 18.12). The
hip is less frequently involved than the knee. Concentric uniform loss of joint
space with axial migration is usual, but superior migration similar to
osteoarthritis may also occur. Acetabular protrusion (protrusio acetabuli) (Figure
18.13), fibrous ankylosis, subchondral cysts, erosions, and secondary reparative
and degenerative changes are common. If steroids are administered,
osteonecrosis of the femoral head is a potential complication. In the foot,
changes may be seen early at the metatarsophalangeal and interphalangeal joints
of the great toe (Figure 18.14). Although the usual changes of rheumatoid
arthritis that are found elsewhere in the skeleton may be present in the foot,
erosions tend to be small and infrequent. Soft-tissue involvement may lead to
hallux valgus and planovalgus deformity of the foot. In the heel, retrocalcaneal
bursitis, Achilles tendonitis, and plantar fasciitis may cause swelling and
calcaneal erosions (Figure 18.15). Spontaneous Achilles tendon rupture may
occur.
•
FIGURE 18.4 Rheumatoid arthritis with juxta-articular osteoporosis.
•
FIGURE 18.5 Hand deformities in rheumatoid arthritis. A and B, Lateral and
posteroanterior radiographs of the hand show a swan neck deformity of the index
finger, boutonniere deformity of the ring finger, a Z-shaped deformity of the thumb,
dislocation of the first carpometacarpal joint, volar dislocation of the
metacarpophalangeal joint of the little finger (arrow in A), dorsal subluxation of the
ulna (arrowhead in A), and ulnar translocation of the carpus (arrowheads in B).
FIGURE 18.6 • Rheumatoid wrist. A, Early findings include juxta-articular

osteoporosis and subtle erosions, including the scaphoid waist (arrow). B, Same
patient 6 years later has severe erosions and subluxations. Ulnar translocation is
present. The bones are diffusely osteoporotic, with no proliferative changes. The
scaphoid waist erosion has become large (arrow).
•
FIGURE 18.7 Rheumatoid arthritis of the carpal bones. A, Coronal T1 MRI shows
erosions. B, Coronal T1 FS Gd MRI shows enhancement in the erosions,
corresponding to inflammatory pannus.
Spine
In the spine, the upper cervical spine is the only common site of involvement. As
many as 70% of patients with rheumatoid arthritis are affected symptomatically
at some time, and up to 85% of those with classic rheumatoid arthritis have
radiographic changes at the upper cervical spine. The atlantoaxial articulation
(C1-C2) has a synovial joint anteriorly where the odontoid process articulates
with the anterior arch of C1 and is stabilized posteriorly by the transverse
ligament. A bursa is interposed between the odontoid process and the transverse
ligament. Synovitis at these sites may cause erosions of the odontoid process and
rupture of the transverse ligament (Figures 18.16 and 18.17), resulting in
widened predental interval. One consequence is atlantoaxial instability, with
imminent danger of quadriplegia or death. Below the level of C2, the cervical
spine may be diffusely involved by joint space narrowing. Inflammatory pannus
at the synovial uncovertebral joints (joints of Luschka) may extend into the
intervertebral disks. The thoracic spine and lumbar spine are usually spared.
Sacroiliac (SI) joint involvement is infrequent and, when present, is mild and
asymmetric.
•
FIGURE 18.8 Rheumatoid arthritis of the left wrist with tenosynovitis. Axial T1 FS
Gd MRI shows thickened synovium with intense contrast enhancement along the
extensor carpi ulnaris (arrow), extensor carpi radialis longus, and brevis tendons
(arrowhead).
•
FIGURE 18.9 Advanced rheumatoid arthritis of the shoulder. An anteroposterior
radiograph shows osteopenia, erosion of the distal clavicle, and remodeling of the
undersurface of the acromion and medial humeral shaft.
Extra-articular Manifestations
Extra-articular manifestations of rheumatoid arthritis include rheumatoid
nodules, development of cutaneous fistulas, infections, hematologic
abnormalities, vasculitis, renal disease, pulmonary disease, and cardiac
complications. Subcutaneous rheumatoid nodules are superficial lesions that
occur in patients with a diagnosis of rheumatoid arthritis. They are considered
one of the most common soft-tissue lesions in these patients, occurring in 20% to
30% of proven cases of rheumatoid arthritis. Pathologically, these lesions are
granulomatous with areas of central necrosis. The presence of rheumatoid
nodules is considered a sign of advanced disease and is generally seen in patients
with a positive RF. The MRI findings of rheumatoid nodules are not specific. On
MRI, rheumatoid nodules are seen as poorly defined masses within the
subcutaneous soft tissues with a central area of necrosis (Figure 18.18).
FIGURE 18.10 • Rheumatoid shoulder with osteoporotic bones and superior

subluxation of the humeral head, indicative of rotator cuff tear or atrophy (arrow).
CONNECTIVE TISSUE DISEASE

Systemic Lupus Erythematosus
SLE is a chronic systemic disease, the pathogenesis of which is related to
immune complex deposition. It is more common in women by an 8:1 ratio, and
there is a component of genetic susceptibility. The fluorescent antinuclear
antibody test is virtually always positive at the onset of clinical disease.
Manifestations in the musculoskeletal system are common and may precede
other systemic manifestations by months or years.6 Nonerosive symmetric
polyarthritis with a distribution similar to rheumatoid arthritis is present in 75%
to 90% of patients with SLE. Early findings on radiographs are fusiform soft-
tissue swelling and juxta-articular osteoporosis, but there should be no joint
space narrowing or erosions. A deforming nonerosive arthropathy is also
common in SLE. The hands are typically involved at the MCP and
interphalangeal joints (Figures 18.19 and 18.20). Thumb, wrist, and foot
involvement are more common than shoulder and knee involvement, and 10% of
patients may develop atlantoaxial subluxation. These deformities are initially
reducible, and radiographs may be normal. Fixed deformities and secondary
degenerative changes may develop with time. Osteonecrosis may involve the
femoral head, femoral condyle, humeral head, and other sites and commonly has
a symmetric distribution. Myositis, tendon weakening and spontaneous rupture,
and soft-tissue calcification are other musculoskeletal manifestations.
•
FIGURE 18.11 Rheumatoid knees. The bones are osteoporotic. Uniform joint space
loss is present with minimal proliferative bone changes. Some secondary
osteoarthritic changes are present in the lateral compartment of the left knee (arrow).
•
FIGURE 18.12 Rheumatoid knee. A, Sagittal T2 FS MRI shows large effusion with
synovial thickening (black arrows). Diffuse cartilage loss and subchondral edema are
present. A large Baker cyst is also present (white arrow). B, Coronal T1 FS Gd MRI
shows synovial and subchondral enhancement.
Scleroderma
Scleroderma (progressive systemic sclerosis) is a multisystem fibrosing
autoimmune connective tissue disease of variable clinical course.
Characteristically, the skin becomes fibrotic, thickened, and taut. Gastrointestinal
and renal involvement is prominent. Radiologic manifestations in the
musculoskeletal system are present in most patients.6,7 These abnormalities are
usually seen in the hands and consist of soft-tissue atrophy, soft-tissue
calcification, resorption of the phalangeal tufts, and distal interphalangeal (DIP)
joint erosions. Osseous destruction and bony erosions are common in the
phalangeal tufts (Figure 18.21). The soft-tissue atrophy results in cone-shaped
fingertips. Subcutaneous calcifications are typically present in multiple digits
and elsewhere in the extremities; the calcium deposits are dystrophic and consist
of calcium hydroxyapatite deposits at sites of local tissue damage. Calcification
may also occur in tendons and tendon sheaths, in joint capsules, and even within
the joint cavity. Synovial fibrosis without inflammation may cause flexion
contractures.
Dermatomyositis and Polymyositis

Dermatomyositis and polymyositis are diseases of unknown etiology affecting
striated muscle by diffuse, nonsuppurative inflammation and degeneration. The
pathogenesis involves an autoimmune mechanism. In dermatomyositis, the skin
is also involved. Multiple clinical classifications are based on various features,
particularly progressive muscle weakness and rash. There is an associated risk of
malignancy in patients older than 40 years with dermatomyositis, especially
men. The diagnosis is made by serum enzyme studies, electromyography, and
muscle biopsy. The early imaging findings of dermatomyositis and polymyositis
can be made on MRI.6 T2 MRI shows high signal in the involved muscles
(Figure 18.22). Involvement is generally symmetric bilaterally, and the course of
the disease can be followed by MRI. On radiographs, the characteristic
abnormality is widespread soft-tissue calcification, particularly of intermuscular
fascial planes between large proximal limb muscles (Figures 18.23 and 18.24).
There may also be subcutaneous calcifications similar to scleroderma (Figure
18.25) or linear calcifications with a reticulated appearance. Muscle atrophy,
contractures, and chronic osteoporosis are findings late in the clinical course.
•
FIGURE 18.13 Rheumatoid hip. Anteroposterior radiograph of the hip shows
concentric uniform loss of joint space with axial migration (protrusio acetabuli, arrow).
•
FIGURE 18.14 Rheumatoid foot. The great toe is deviated laterally, and the
remaining metatarsophalangeal (MTP) joints are subluxated. Erosions are present at
all the MTP joints and the interphalangeal joint of the great toe; the other joints appear
spared. Some erosions appear sclerotic (arrow), suggesting clinical quiescence.
•
FIGURE 18.15 Rheumatoid arthritis. Swelling of the retrocalcaneal bursa is present
(black arrow). Multiple bony erosions are seen in the calcaneus (white arrow).
•
FIGURE 18.16 Rheumatoid arthritis. Atlantoaxial subluxation is present with a wide
gap between the anterior arch of C1 and the odontoid process (black arrow).
•
FIGURE 18.17 Rheumatoid arthritis. Sagittal T2 MRI shows pannus (arrow) eroding
the odontoid process and causing mass effect on spinal cord.
Overlap Syndromes
Patients may have rheumatic diseases with clinical features that overlap those of
several of the more well-defined rheumatoid diseases, particularly at the
beginning or end of the clinical course. The radiographic features of disease may
also overlap so that an individual case may show combinations of features of
rheumatoid arthritis, scleroderma, SLE, and dermatomyositis. These overlap
syndromes may also be called mixed connective tissue disease.
SPONDYLOARTHRITIS (SPONDYLOARTHROPATHY)
Spondyloarthritis (also called spondyloarthropathy) comprises a heterogeneous
group of interrelated conditions.8 Musculoskeletal manifestations common to
these diseases include spinal involvement, especially of the SI joints,
enthesopathy, and asymmetric peripheral arthritis of the lower limbs. Additional
common features are genetic predisposition; extra-articular manifestations in the
skin, gut, urogenital tract, or eyes; negative serum RF; and an association with
HLA-B27. These conditions have in the past been called rheumatoid variants to
distinguish them from rheumatoid arthritis and seronegative
spondyloarthropathy to reflect the negative serum RF.
•
FIGURE 18.18 Rheumatoid nodule in a foot. A, Coronal T1 MRI of the foot at the
level of metatarsophalangeal joint shows a lobulated insinuating mass between the
third and fourth metatarsals. The mass shows iso–signal intensity to the muscle. B,
Coronal T2 FS MRI shows heterogeneous high signal intensity (arrows). C, Coronal
T1 FS Gd MRI shows intense, heterogeneous enhancement of the mass with areas of
nonenhanced portion that correspond to areas of necrosis (arrow).
Axial Spondyloarthritis and Ankylosing Spondylitis

Axial spondyloarthritis is a common chronic inflammatory disease of the spine
and SI joints8; ankylosing spondylitis is considered an extreme subset of axial
spondyloarthritis.8 The etiology is unknown, but there is a genetic component;
90% to 95% of white patients with classic ankylosing spondylitis have HLA-
B27 (compared with 9% of all white patients). Axial spondyloarthritis affects
approximately 1% of the general adult population in the United States8; the
prevalence of ankylosing spondylitis is approximately 0.1%. The typical onset is
insidious lower back pain and stiffness in adolescent men. In the severe classic
form, there is gross ankylosis and deformity of the spine; in mild forms, there
may be only occasional arthralgias. In most cases, axial spondyloarthritis is a
benign, self-limited, and undiagnosed disease with absent or minimal
radiographic changes. The overall sex distribution is probably equal, but men
generally have severe, progressive disease, whereas women have mild, self-
limited disease.
•
FIGURE 18.19 Systemic lupus erythematosus with alignment deformities. A and B,
Lateral and posteroanterior radiographs show swan neck deformities of the ring and
little fingers, with proximal interphalangeal hyperextension of the middle finger.
•
FIGURE 18.20 Systemic lupus erythematosus with severe subluxations at the
metatarsophalangeal joints. Erosions are absent.
•
FIGURE 18.21 Scleroderma with calcium hydroxyapatite deposits in thumb and
atrophy of the soft tissues.
FIGURE 18.22 • Inflammatory myositis. Axial T2 FS MRI shows high signal
intensities symmetrically distributed in the thigh muscles.
•
FIGURE 18.23 Dermatomyositis at the ankle with soft-tissue calcification.
Disease involvement of the spine typically starts at the thoracolumbar or

lumbosacral junctions. The first radiographic evidence of spine involvement
occurs where the annulus fibrosus outer fibers attach to the vertebral body.5,9,10
Small erosions occur with the development of adjacent sclerosis. The erosions
are known as Romanus lesions (Figure 18.26A). Next, either new bone
formation occurs along the anterior aspect of the vertebral body, or the corner
erosions progress, leading to a barrel-shaped or square vertebral body on the
lateral radiographic view of the spine (Figure 18.26B). As the disease continues
to progress, ossifications in and around the periphery of the annulus fibrosus
form (Figure 18.26C); these ossifications are called syndesmophytes. The facet
joints become inflamed and then ankylosed. Syndesmophytes at multiple
contiguous levels lead to a spine that looks like bamboo (Figure 18.27).
Back pain diminishes or disappears as the spine fuses, but the fused spine
becomes osteoporotic, fragile, and subject to insufficiency fractures. In the
pelvis, the SI joints become symmetrically blurred, sclerotic, and fused (Figure
18.28). Early in this process, the SI joints have subchondral granulation tissue,
and the joint cartilage becomes replaced by fibrous tissue. Ankylosis follows the
formation of new cartilage and bone in the joint space.
•
FIGURE 18.24 Dermatomyositis at the knee with prominent soft-tissue calcification
around the quadriceps muscles.
•
FIGURE 18.25 Polymyositis with soft-tissue calcification (arrow) involving the index
finger.
Approximately 20% of patients with ankylosing spondylitis present initially

with peripheral polyarthritis, and, ultimately, approximately 35% will have
peripheral disease. This peripheral polyarthritis is similar to rheumatoid arthritis
in clinical manifestations, radiographic appearance, and pathophysiology, but the
distribution of disease tends to be different. The feet, ankles, knees, hips, and
shoulders are typically involved in an asymmetric fashion; the hands are usually
spared. Permanent stiffness or bony ankylosis is likely. Peripheral polyarthritis
may precede, coincide with, or follow the onset of spinal manifestations.
•
FIGURE 18.26 Ankylosing spondylitis in lumbar spines (different patients). A-C,
Lateral radiographs of the lumbar spines demonstrate early erosion with sclerosis
(arrow in A), squaring (arrows in B) of the anterior aspects of the lumbar vertebral
bodies, and syndesmophyte formation along the anterior annulus fibrosus (arrow in
C).
•
FIGURE 18.27 Ankylosing spondylitis of the lumbar spine. A and B, Anteroposterior
and lateral radiographs show syndesmophytes and ossification of the posterior
ligamentous structures forming a bamboo spine. The sacroiliac joints have fused.
MRI is more sensitive than radiography in the early detection of sacroiliitis.

MRI findings of sacroiliitis include abnormal cartilage signal intensity, erosions,
increased intensity in the joint, and subchondral bone marrow edema (Figure
18.29). MRI may also be able to distinguish sacroiliitis due to
spondyloarthropathy from septic arthritis of the SI joint.
A major orthopedic complication of ankylosing spondylitis is increased
biomechanical fragility of the spine. Syndesmophytes bridging the vertebral
bodies and ankylosis of the posterior elements result in a stiff spine that cannot
move or dissipate traumatic forces. Bony remodeling of an ankylosed spine does
not improve its biomechanical strength as a unit. When patients with ankylosing
spondylitis are involved in falls or other accidents, fractures and fracture-
dislocations of the spine are common (Figure 18.30). These fractures may
progress to nonunion.
•
FIGURE 18.28 Ankylosing spondylitis with symmetric, inflammatory arthritis of the
hips, ankylosis of the sacroiliac joints, and hyperostosis at the ischial rami.
•
FIGURE 18.29 Ankylosing spondylitis with symmetric inflammatory sacroiliitis. Axial
T2 FS MRI shows subchondral edema in both sacroiliac joints (arrows).
Reactive Arthritis
Reactive arthritis is an acute inflammatory arthritis that is triggered by an
infection elsewhere in the body,11 but infectious organisms cannot be cultured
from the joint fluid or synovium, distinguishing the condition from infectious
arthritis. The pathogenesis of the disease is thought to be immunologic in nature,
with a genetic predisposition; it is classified as a spondyloarthropathy. After
gastrointestinal infections by Shigella, Salmonella, Yersinia, or Campylobacter,
or a genitourinary infection with Chlamydia, approximately 1% to 4% of
patients develop reactive arthritis. Although the triad of peripheral arthritis,
conjunctivitis, and urethritis has been classically associated with reactive
arthritis, the current definition generally includes cases of arthritis that occur
within 2 months of an episode of venereal infection or epidemic dysentery. The
classic triad is present in only one-third of cases of reactive arthritis. The
diagnosis may be difficult to make because there is no definite laboratory test,
and the dysenteric or venereal episode may be mild or silent. There is a marked
male predominance of at least 5:1. The typical age of onset is 15 to 40 years.
HLA-B27 is present in 70% to 80% of cases, and the serum RF is negative.
Clinically, reactive arthritis is an asymmetric lower extremity oligoarthritis
manifested by sausage digits, heel pain and swelling, low back pain, and SI joint
tenderness. Early clinical signs include effusion, periarticular edema, bursitis,
and tendinitis. Fluffy periostitis, enthesopathy, paravertebral comma-shaped
ossification, and asymmetric sacroiliitis often develop. Bone density is preserved
in chronic disease.
•
FIGURE 18.30 Ankylosing spondylitis with traumatic cervical spine fracture at C5-
C6 (arrow).
Radiographic abnormalities develop in 60% to 80% of cases, with

involvement of synovial joints, symphyses, and enthuses.10,11 The disease has a
predilection for the foot—especially the great toe, ankles, knees, and SI joints—
and manifestations are rarely seen above the level of the umbilicus. Bony
erosions combined with bony proliferation characterize an asymmetric arthritis.
Erosions first appear at the joint margins and may progress to involve the
subchondral bone in the central portion of the articulation. Bony proliferation
may take the form of periostitis (linear or fluffy), calcification and ossification at
entheses, and intra-articular bone production with bony ankylosis. Additional
abnormalities may include fusiform soft-tissue swelling, effusions, regional or
periarticular osteoporosis, and symmetric and concentric joint space narrowing.
Sacroiliitis is the most common manifestation. The incidence of sacroiliitis
increases with chronicity of disease, rising from 5% to 10% of cases at onset to
perhaps 75% after several years. Sacroiliitis is evident on radiographs as
erosions and sclerosis of the adjacent sacral and iliac articular surfaces, initially
worse on the iliac side (Figure 18.31). Bilateral changes are typical, and these
may be symmetric or asymmetric.
Spinal involvement in reactive arthritis is much less frequent than in
ankylosing spondylitis or psoriasis. Asymmetric paravertebral ossification about
the lower 3 thoracic and upper 3 lumbar vertebrae in reactive arthritis is
indistinguishable from the corresponding changes in psoriatic spondylitis. These
ossifications are thought to result from inflammatory changes in the
paravertebral connective tissue that lead to calcification and ossification. Unlike
ankylosing spondylitis, squaring of the vertebral bodies, facet joint erosion,
sclerosis, and osseous fusion are unusual in reactive arthritis.
•
FIGURE 18.31 Reactive arthritis with sacroiliitis, greater on the left (arrow).
•
FIGURE 18.32 Psoriatic arthritis with “sausage digit” swelling, erosions (long
arrow), and periostitis (short arrow) of the index finger.
Psoriatic Arthritis
Psoriasis is a common skin disease characterized by dry, pink, scaly, nonpruritic
lesions with a genetic predisposition. As many as 30% of patients with psoriasis
develop an associated arthritis.12 The onset and clinical course of skin lesions
and arthritis are generally asynchronous and independent, but 80% to 85% have
skin involvement first. Psoriatic arthritis seems to be heritable but related to
multiple genes, with the disease triggered by some interaction between genetic
and environmental factors. HLA-B27 is found in 60% to 80% of patients with
psoriatic spondylitis but in only 20% of patients with psoriatic peripheral
arthritis. Serum RF is typically absent. Psoriatic arthritis has 5 patterns of
clinical presentation: (1) asymmetric oligoarthritis, seen in more than 50% of
cases; (2) polyarthritis with predominantly DIP joint involvement, the classic
presentation, which is seen in 5% to 19%; (3) symmetric seronegative
polyarthritis simulating rheumatoid arthritis, seen in up to 25%; (4) sacroiliitis
and spondylitis resembling ankylosing spondylitis, seen in 20% to 40%; and (5)
arthritis mutilans with resorption of phalanges, seen in 5%. Individual patients
may change from one clinical pattern to another. Two-thirds of patients have an
insidious onset, whereas one-third have an acute onset mimicking gout or septic
arthritis. The age of onset is 35 to 45 years, and there is no sex predominance.
Important clinical features include joint tenderness and swelling, spine pain and
range of motion, enthesitis, and dactylitis.
The predominant radiologic abnormalities are found asymmetrically in the
upper extremities and result from a synovitis that is similar in pathophysiology
to rheumatoid arthritis. The distribution of articular involvement in the hands
tends to be distal, commonly the DIP joints of the fingers, and usually
accompanies fingernail involvement. Soft-tissue swelling of the digits tends to
be of the “sausage” variety, in which the entire digit is swollen, not just the
joints; this swelling represents dactylitis (Figure 18.32). Dramatic joint space
loss to the point of erosion and resorption of the articulating ends of bones may
occur. Pencil-in-cup erosions (Figure 18.33) and periosteal bony excrescences
(Figure 18.34) are other typical findings. The arthritis is highly erosive and, in
the hands or feet, may lead to arthritis mutilans, which is severe resorptive
arthritis of the phalanges (Figures 18.35 and 18.36). Periostitis and entheseal
bone proliferation may be found. When acute, periostitis may be fluffy and
irregular; when healed, it may enlarge the bone. In the spine, irregular,
asymmetric paravertebral excrescences of bone appear; these may be bulky and
merge with the underlying vertebral bodies and disks (Figure 18.37). The
changes in the spine and SI joints in psoriatic arthritis tend to be more marked
than those in reactive arthritis, but they are often indistinguishable. Sacroiliitis
may progress to ankylosis.
FIGURE 18.33 • Psoriatic arthritis with interdigitating erosions (pencil-in-cup
appearance).
•
FIGURE 18.34 Psoriatic arthritis with inflammatory periostitis (arrows).
•
FIGURE 18.35 Psoriatic arthritis in the feet. Most of the distal interphalangeal joints
are severely involved and subluxated.
•
FIGURE 18.36 Arthritis mutilans presentation of psoriatic arthritis in the hand and
wrist. The distal interphalangeal and proximal interphalangeal joints of all the fingers
are severely involved. There is pancompartmental involvement of the wrist, with
erosions and mature periosteal bone.
•
FIGURE 18.37 Psoriatic arthritis in the spine and sacroiliac joints. Anteroposterior
radiograph of the lumbar spine shows asymmetric paravertebral ossification and large
bony bridging. Both sacroiliac joints are ankylosed.
Enteropathic Spondyloarthropathy
Patients with inflammatory bowel disease (Crohn disease, ulcerative colitis) and
other gastrointestinal conditions may have spondyloarthropathy associated with
their disease.13 The prevalence of articular disease in patients with inflammatory
bowel disease may be as high as 20%, and it may occur before, simultaneously
with, or following the onset of the gastrointestinal disease. Common articular
manifestations include peripheral joint arthralgias, soft-tissue swelling, and
periarticular osteoporosis; less common manifestations include erosive changes
similar to rheumatoid arthritis. The peripheral arthritis may wax and wane in
tandem with exacerbations and remissions in the bowel disease. Sacroiliitis and
spondylitis resembling or identical to ankylosing spondylitis may also occur in
inflammatory bowel disease, more commonly in patients with Crohn disease
than in those with ulcerative colitis. The sacroiliitis and spondylitis tend to be
progressive and not particularly related to the bowel disease (Figure 18.38).
Certain dysenteric infections are associated with reactive arthritis, as discussed
earlier in this chapter.
Differential Diagnosis
Although the spondyloarthropathies have common features, it is frequently
possible to distinguish one from the other in individual patients (Table 18.1). The
manifestations of ankylosing spondylitis are usually severe in the spine and SI
joints and less severe in the peripheral joints. The manifestations of psoriatic
arthritis are usually severe in the small peripheral joints and less severe in the
large peripheral joints, spine, or SI joints. The manifestations of reactive arthritis
are usually mild and rarely involve the upper body. When disease is mild and
radiographic findings are minimal, it may be difficult to recognize a specific
form of spondyloarthropathy.
JUVENILE IDIOPATHIC ARTHRITIS

Juvenile idiopathic arthritis is a heterogeneous group of idiopathic inflammatory
joint conditions with onset before the age of 16 years, a designation that includes
the conditions formerly called juvenile rheumatoid arthritis and juvenile chronic
arthritis. In adults, the radiologic sequelae of juvenile idiopathic arthritis reflect
the effect of chronic inflammatory arthritis on the growing skeleton. These
sequelae may include permanent muscle wasting; bone dysplasia from
epiphyseal overgrowth, cartilage loss, and early growth plate closure; loss of
function from ankylosis and joint contractures; and secondary osteoarthritis
(Figures 18.39–18.41). The earlier the onset of disease, the more severe the
growth effects. Involvement may be symmetric, asymmetric, or monarticular.
Even though the arthritis itself may remit by adulthood,14 the orthopedic
complications may continue to require treatment throughout life.
•
FIGURE 18.38 Unilateral inflammatory sacroiliitis in a patient with inflammatory
bowel disease. Axial CT shows erosions of the left sacroiliac joint (arrows).
Table 18.1 DISTINGUISHING FEATURES OF SPONDYLOARTHROPATHY
Ankylosing Reactive
Feature Spondylitis Arthritis Psoriatic Arthritis
Clinical Low-back pain, Following Psoriasis (skin
setting adolescents dysenteric or disease)
venereal
infection
Sex Male (classic Male None
predominance disease)
Joint Sacroiliac (SI), SI, lumbar Hands, feet,
distribution entire spine spine, feet thoracolumbar
spine
Severity of Severe ankylosis Mild Severe erosions
involvement
SI joint Bilateral, symmetric Bilateral, Bilateral,
involvement sacroiliitis invariably asymmetric asymmetric
leading to ankylosis sacroiliitis sacroiliitis, may
progress to
ankylosis
Type of Delicate Paravertebral Paravertebral
phytes syndesmophytes ossification ossification
•
FIGURE 18.39 Sequelae of juvenile idiopathic arthritis in a young adult. A, The left
hand had ankylosis of the radius with the scaphoid and lunate. The ulnar head is
dysplastic. B, The right hand shows pancarpal ankylosis with secondary degenerative
changes at the radiocarpal and carpometacarpal joints.
•
FIGURE 18.40 Sequelae of juvenile idiopathic arthritis in a young adult. Osteopenia
is severe. A, The hand has dysplastic bones in which growth plates fused
prematurely. B, In the foot, the tarsal bones are fused and dysplastic.
•
FIGURE 18.41 Sequelae of juvenile idiopathic arthritis involving the hips of a young
adult. Radiograph shows diffuse joint space narrowing, secondary dysplasia, and
superimposed degenerative changes.
References
1. Scott DL, Wolfe F, Huizinga TW. Rheumatoid arthritis. Lancet. 2010;376(9746):1094–1108.
doi:10.1016/S0140-6736(10)60826-4 [PMID:20870100].
2. Resnick D, ed. Diagnosis of Bone and Joint Disorders. 4th ed. Philadelphia: Saunders; 2002.
3. Sommer OJ, Kladosek A, Weiler V, Czembirek H, Boeck M, Stiskal M. Rheumatoid arthritis: a practical
guide to state-of-the-art imaging, image interpretation, and clinical implications. RadioGraphics.
2005;25:381–398.
4. Burge AJ, Nwawka OK, Berkowitz JL, Potter HG. Imaging of inflammatory arthritis in adults: status
and perspectives on the use of radiographs, ultrasound, and MRI. Rheum Dis Clin North Am.
2016;42(4):561–585. doi:10.1016/j.rdc.2016.07.001 [PMID:27742015].
5. Jacobson JA, Girish G, Jiang Y, Resnick D. Radiographic evaluation of arthritis: inflammatory
conditions. Radiology. 2008;248(2):378–389. doi:10.1148/radiol.2482062110 [PMID:18641245].
6. Kolasinski SL, Chi AS, Lopez-Garib AJ. Current perspectives on imaging for systemic lupus
erythematosus, systemic sclerosis, and dermatomyositis/polymyositis. Rheum Dis Clin North Am.
2016;42(4):711–732. doi:10.1016/j.rdc.2016.07.007 [Epub September 9, 2016. PMID:27742023].
7. Boutry N, Hachulla E, Zanetti-Musielak C, Morel M, Demondion X, Cotten A. Imaging features of
musculoskeletal involvement in systemic sclerosis. Eur Radiol. 2007;17(5):1172–1180 [Epub
September 23, 2006. PMID:17021702].
8. Taurog JD, Chhabra A, Colbert RA Ankylosing spondylitis and axial spondyloarthritis. N Engl J Med.
2016;374(26):2563–2574. doi:10.1056/NEJMra1406182 [PMID:27355535].
9. Resnick D. Radiology of seronegative spondyloarthropathies. Clin Orthop Relat Res. 1979(143):38–45
[PMID:509835].
10. Resnik CS, Resnick D. Radiology of disorders of the sacroiliac joints. JAMA. 1985;253(19):2863–2866
[PMID:3989961].
11. Schmitt SK. Reactive arthritis. Infect Dis Clin North Am. 2017;31(2):265–277.
doi:10.1016/j.idc.2018.01.002 [Epub March 11, 2017. PMID:28292540].
12. Ritchlin CT, Colbert RA, Gladman DD. Psoriatic arthritis. N Engl J Med. 2017;376(10):957–970.
doi:10.1056/NEJMra1505557. Erratum in: N Engl J Med. 2017;376(21):2097 [PMID:28273019].
13. Peluso R, Di Minno MN, Iervolino S, et al. Enteropathic spondyloarthritis: from diagnosis to treatment.
Clin Dev Immunol. 2013;2013:631408. doi:10.1155/2013/631408 [Epub April 15, 2013.
PMID:23690825; PMCID:PMC3649644].
14. Shoop-Worrall SJW, Kearsley-Fleet L, Thomson W, Verstappen SMM, Hyrich KL. How common is
remission in juvenile idiopathic arthritis: a systematic review. Semin Arthritis Rheum. 2017. pii:S0049–
0172(17)30123-3. doi:10.1016/j.semarthrit.2018.05.007 [Epub ahead of print. PMID:28625712].
1. Which of the following radiographic features is most likely to be seen in

osteoarthritis?
A. Ankylosis
B. Juxta-articular osteoporosis
C. Marginal erosions
D. Subchondral cysts
2. Which radiographic feature is most characteristic of osteoarthritis in the

hands?
A. Osteophytes
B. Subluxation
C. Chondrocalcinosis
D. Erosions
3. Which of the following joints is most commonly affected by osteoarthritis?

A. Radiocarpal
B. First carpometacarpal
C. Scapholunate
D. Pisotriquetral
4. Enthesophytes are most closely associated with which condition?
A. Inflammatory osteoarthritis
B. Baastrup disease
C. Intervertebral disk degeneration
D. Diffuse idiopathic skeletal hyperostosis

1. D Subchondral cysts are found in osteoarthritis, but the other features are
generally not.
2. A Osteophytes are the characteristic radiographic feature of osteoarthritis.
3. B The first carpometacarpal joint is the joint most commonly affected by
osteoarthritis among the options.
4. D Enthesophytes are most closely associated with diffuse idiopathic skeletal
hyperostosis.
19
Noninflammatory Joint Disease
This chapter covers various joint diseases that have predominantly

noninflammatory features on radiographs. Osteoarthritis is covered in chapter
15.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of noninflammatory joint disease, the
4. summarize relevant concepts and knowledge for the following topics: neuropathic
osteoarthropathy, pyrophosphate arthropathy, hydroxyapatite deposition disease, gouty arthritis
and tophaceous gout, multicentric reticulohistiocytosis, amyloid arthropathy, pigmented
villonodular synovitis, synovial chondromatosis, posttraumatic osteolysis of the distal clavicle,
Baker cyst, femoroacetabular impingement, shoulder impingement, rotator cuff tear
arthropathy, and lipoma arborescens.
NEUROPATHIC OSTEOARTHROPATHY
Neuropathic joint (Charcot joint) refers to a pattern of destructive joint
osteoarthropathy due to a loss of proprioception and deep pain sensation.
Continued use of the joint can lead to rapidly progressive erosion of the articular
cartilage, reactive subchondral sclerosis, fractures, and fragmentation of
subchondral bone, ending with a severely disorganized joint. Joint debris induces
synovitis and chronic effusion. The damage and derangement may occur over a
period of days to weeks with relatively little symptomatology. Neuropathic
osteoarthropathy results from both lower motor neuron (peripheral) and upper
motor neuron (central) lesions.
Diabetic peripheral neuropathy is the most common lower motor neuron
lesion; other etiologies include alcoholism, tuberculosis, amyloidosis, leprosy,
peripheral nerve trauma, steroids, and congenital indifference to pain.
Neuropathic osteoarthropathy occurs in 0.1% of all diabetics and in 5.0% of
those with diabetic neuropathy. The most frequent site of involvement is the foot
(80%), especially the tarsometatarsal, intertarsal, and metatarsophalangeal
(MTP) joints; involvement may be unilateral or bilateral. Tarsometatarsal
fracture-dislocation may occur spontaneously or with minimal trauma. Extensive
sclerosis, osteophytosis, fractures, bony fragmentation, subluxation, dislocation,
bony debris, effusion, and subchondral cysts are common findings (Figure 19.1).
MRI will show marrow edema and joint effusion.1,2
Syringomyelia is the most common upper motor neuron lesion to result in
neuropathic osteoarthropathy; other etiologies include meningomyelocele,
trauma, multiple sclerosis, tabes dorsalis (syphilis), and cord compression.
Neuropathic osteoarthropathy occurs in 25% of patients with syringomyelia. The
joint changes are usually in the upper extremity (80%), and they may be atrophic
rather than proliferative. Acute resorption of the articulating ends of the bone
without evidence of repair, gross soft-tissue swelling, or bony debris in the soft
tissues is a common finding. This process may mimic destruction from tumor or
infection.2 The most commonly involved joint is the glenohumeral joint (Figure
19.2).
CRYSTAL-ASSOCIATED DISEASES
Crystal-associated joint diseases are pathologic conditions that occur in the
presence of crystals.3 The crystals contribute to tissue damage, but the causal
relationship between crystals and tissue damage is not well understood. Crystals
precipitate from the extracellular fluid space and accumulate in the articular
tissues. Deposits of crystals may then be shed episodically into the joint space.
Clearance of crystals from the joint space and articular cartilage is poor because
these structures are avascular and alymphatic and have few scavenger cells. The
presence of particles alters the mechanical properties of the tissues, tending to
make them less elastic. Articular cartilage becomes particularly vulnerable to
damage and ultimately undergoes degenerative changes. Large crystalline
particles in the joint space can cause direct abrasive damage to the articular
surfaces. Small particles can cause damage by biophysical and biochemical
interactions with cell membranes and macromolecules and may also provoke an
acute synovitis. Crystal-induced inflammatory reactions tend to have a sudden
onset and a rapid, self-limited course. The sudden onset is probably related to the
abrupt shedding of crystals into the joint space from a deposit in the articular
tissues.
•
FIGURE 19.1 Neuropathic osteoarthropathy. Sagittal T1 MRI of the foot shows
swelling, disorganization, and edema of the midfoot.
•
FIGURE 19.2 Neuropathic shoulder joint in a patient with syringomyelia. Frontal
radiograph of left shoulder shows bony fragmentation, dislocation, debris, and
sclerosis.
Table 19.1 CRYSTAL DEPOSITION DISEASES OF JOINTS
Crystal Associated Clinical Conditions

Calcium pyrophosphate Chondrocalcinosis
dihydrate Pseudogout
Pyrophosphate arthropathy
Calcium hydroxyapatite Asymptomatic calcification
Calcific tendonitis, bursitis, and
periarthritis
Chronic destructive joint disease
Monosodium urate Hyperuricemia
monohydrate Gouty arthritis
Tophaceous gout
Table 19.2 CLINICAL SYNDROMES OF CALCIUM PYROPHOSPHATE DIHYDRATE

DEPOSITION DISEASE
Asymptomatic Chondrocalcinosis
Acute Crystal Synovitis
Acute, intermittent (pseudogout)
Subacute or chronic (resembles rheumatoid arthritis)
Pyrophosphate Arthropathy (Resembles Osteoarthritis)
Without attacks of pseudogout
With intermittent attacks of pseudogout
Neuropathiclike (resembles neuropathic osteoarthropathy)
Crystal deposition diseases have 3 clinical presentations: (1) an asymptomatic

state in which crystals can be detected, (2) an inflammatory arthritis, and (3) a
chronic destructive arthropathy. The particular diseases are defined by the
presence of characteristic crystals within affected joints. Aspiration of the joint
during an acute inflammatory episode may yield a material in which the
associated crystal can be demonstrated. The 3 types of crystals that are
commonly associated with joint diseases are calcium pyrophosphate dihydrate
(CPPD), calcium hydroxyapatite, and monosodium urate monohydrate (Table
19.1).
Calcium Pyrophosphate Dihydrate Crystal Deposition Disease

CPPD crystal deposition disease is a polyarticular arthritis with deposition of
CPPD crystals in articular tissues.4 However, its initial presentation may be
monoarticular. The definitive clinical diagnosis requires the identification of
CPPD crystals from joint fluid, but the radiologic findings can be diagnostic.
CPPD deposition disease has been associated with hyperparathyroidism,
hemochromatosis, aging, and osteoarthritis. It has been weakly associated with
hypothyroidism, ochronosis, Paget disease, Wilson disease, acromegaly,
diabetes, and gout. CPPD crystal deposition disease has 3 manifestations:
chondrocalcinosis, crystal-induced synovitis, and pyrophosphate arthropathy
(Table 19.2).
CPPD crystals are generated locally in the articular tissues, where
asymptomatic deposits may accumulate in cartilage, joint capsules, intervertebral
disks, tendons, and ligaments. In cartilage, these deposits may be evident
radiographically as chondrocalcinosis. Chondrocalcinosis is most common in the
knees, wrists, elbows, and hips and is found in both fibrocartilage and hyaline
cartilage. Chondrocalcinosis in the menisci can mimic a meniscal tear on MRI.
Chondrocalcinosis in the hyaline cartilage appears as linear or punctate areas of
low signal, which become more noticeable on GRE MRI owing to blooming
artifact.
Shedding of crystals into the joint space after rupture of a deposit causes an
acute, self-limited, crystal-induced synovitis. This acute synovitis is clinically
similar to acute gouty arthritis and has been known as pseudogout. As with
gouty arthritis, acute episodes of inflammatory synovitis may recur
intermittently. During an acute episode, CPPD crystals may be recovered by
joint aspiration and identified by polarized light microscopy. Uncommonly, these
episodes can run together into a subacute or chronic crystal synovitis that
resembles rheumatoid arthritis, except that the large joints of the limbs tend to be
involved rather than the hands and feet.
Pyrophosphate arthropathy is the degenerative result of structural joint
damage caused by chronic CPPD crystal deposition and irreversible destruction
of the articular cartilage. The degenerative changes can be identical to
osteoarthritis, but the distribution of involvement is different. In the hand, the
metacarpophalangeal joints are characteristically involved. In the wrist, the
radiocarpal joint is characteristically involved. In severe cases, the process
causes gross scapholunate dissociation in association with degenerative
radiocarpal changes. The scaphoid and lunate separate, and the capitate migrates
proximally into the resulting gap. This syndrome is called scapholunate
advanced collapse wrist (Figures 19.3 and 19.4). The scapholunate advanced
collapse wrist usually includes pancompartmental degenerative involvement.
The shoulder (glenohumeral), knee (especially patellofemoral), elbow, ankle,
and foot (talonavicular) are the other common sites of involvement (Figure
19.5). Chondrocalcinosis need not be present and is absent if there is no
remaining cartilage. Isolated severe involvement of the patellofemoral
compartment of the knee or selective radiocarpal involvement of the wrist is
virtually diagnostic of pyrophosphate arthropathy (Figure 19.6). Pyrophosphate
arthropathy is often, but not necessarily, combined with acute episodes of
crystal-induced synovitis. Very severe degenerative changes may lead to an
appearance that resembles neuropathic osteoarthropathy.
•
FIGURE 19.3 Pyrophosphate arthropathy with scapholunate advanced collapse
wrist. Chondrocalcinosis involves the triangular fibrocartilage complex (arrow).
Hydroxyapatite Deposition Disease

Hydroxyapatite deposition disease is a heterogeneous group of conditions that
have in common the abnormal presence of amorphous hydroxyapatite (basic
calcium phosphate) crystals in the soft tissues.5 Ion contaminants such as
carbonate, magnesium, fluoride, and chloride are present. The etiology and
pathogenesis of hydroxyapatite deposition disease are not well understood.
There may be multiple causes and multiple mechanisms of deposition. The
radiologic manifestations of hydroxyapatite deposition disease are similar to
other crystal-associated conditions: asymptomatic deposits, acute crystal-
induced synovitis, and chronic destructive arthropathy. Unlike CPPD deposition
disease, hydroxyapatite deposition disease typically involves the tendons,
ligaments, joint capsules, and other periarticular soft tissues (Figures 19.7–
19.10) rather than the articular cartilage and subchondral bone.
Deposits of hydroxyapatite in the soft tissues appear on radiographs as dense,
homogeneous, sharply marginated, and amorphous calcifications. The
calcifications may have linear, angular, or round shapes, and unlike
chondrocalcinosis, they do not conform to cartilage structures. Occasionally,
deposits may mimic mineralized osteoid tumor matrix. A minority of patients
with hydroxyapatite deposits have symptoms. The soft-tissue calcifications of
immune-mediated connective tissue diseases such as scleroderma, polymyositis,
and dermatomyositis are also in the form of hydroxyapatite, as are the metastatic
soft-tissue deposits (periarticular calcinosis, tumoral calcinosis) associated with
chronic kidney disease. Intratendinous calcifications may be difficult to detect on
routine MRI sequences because they may be isointense to tendons. Blooming
may occur with GRE MRI, and muscle and soft-tissue edema may be present.
Recurrent episodes of calcific tendonitis or calcific bursitis are common with
hydroxyapatite deposits. Most patients are in their 40s and 50s and present with
acute pain, swelling, and tenderness. Symptoms respond rapidly to a
nonsteroidal anti-inflammatory agent. The shoulder, particularly the
supraspinatus tendon, is a common site of involvement. Tendons may atrophy
and rupture, but it is unclear whether the deposits initially caused the local tissue
damage or preexisting tissue damage allowed the deposits to accumulate. The
deposits around the shoulder are bilateral in approximately half of cases and may
migrate to contiguous structures. After clinical resolution, the deposits may
disappear. The process is usually monarticular, but multiple joints may be
involved at the same time or successively. Other common sites of involvement
include the long head of the biceps tendon, the extensors of the wrist, the
myotendinous attachments along the linea aspera (thigh adductors) and at the
medial border of the proximal tibia (pes anserinus), the olecranon bursa, the
trochanteric bursa, and the ischial bursa.
Hydroxyapatite crystals have been associated with a chronic destructive
arthritis similar to osteoarthritis or CPPD deposition disease. This situation is
relatively uncommon and most often occurs in the setting of renal failure and
hyperparathyroidism (Figure 19.11). Mixtures of crystals may be recovered from
such joints, including CPPD and hydroxyapatite.
•
FIGURE 19.4 Calcium pyrophosphate dihydrate crystal deposition of the hand. A,
Posteroanterior radiograph shows joint space narrowing (arrows) at the index and
middle metacarpophalangeal (MCP) joints. B, Coronal T2 FS MRI shows high signal
(arrows) at the index and middle MCP joints. C, Coronal T1 FS Gd MRI shows
enhancement (arrows) at the index and middle MCP joints.
Gout
Gout is defined by the presence of hyperuricemia (elevated serum uric acid
level).6 Hyperuricemia may be idiopathic or secondary to known conditions,
including excess ingestion (in protein), intrinsic overproduction, or reduced renal
secretion. There is a familial incidence that appears to be controlled by multiple
genes. Specific mutations with biochemical defects in purine metabolism leading
to hyperuricemia have been found in a few cases. Gout is associated with
obesity, diabetes, hyperlipidemia, hypertension, atherosclerosis, alcohol
consumption, acute illness, and pregnancy. There is a negative association with
rheumatoid arthritis. The prevalence of the symptomatic forms of gout, gouty
arthritis, and tophaceous gout has declined dramatically with the increasing use
of drugs that control hyperuricemia. Gouty arthritis is similar to other crystal-
related joint diseases, whereas tophaceous gout has the radiology of a metabolic
deposition disease (discussed in the Metabolic Deposition Disease section).
FIGURE 19.5 • Pyrophosphate arthropathy of the shoulder with prominent

osteophyte formation (arrow), loss of joint space, subchondral cysts, and superior
subluxation of humeral head.
•
FIGURE 19.6 Pyrophosphate arthropathy of the knee. Posteroanterior radiograph
shows chondrocalcinosis at medial and lateral menisci (arrows).
•
FIGURE 19.7 Calcium hydroxyapatite deposit in the supraspinatus tendon of the
rotator cuff (arrow).
•
FIGURE 19.8 Hydroxyapatite deposit (arrow) in the subscapularis tendon of the
rotator cuff shown on axial GRE MRI.
Gouty arthritis is the articular disease associated with monosodium urate

monohydrate, the crystalline form in which uric acid is precipitated from
solution into the soft tissues. The age of peak onset of gouty arthritis is 50 years,
and it develops only after decades of sustained hyperuricemia. Approximately
90% of cases occur in men. Gouty arthritis commonly presents as an acute
crystal-induced synovitis that tends to be recurrent and episodic. Radiographs
may show only fusiform soft-tissue swelling unless there are concurrent features
of tophaceous gout. Urate crystals shed into the synovial fluid or synovial tissues
provoke an acute inflammatory synovitis. A chronic destructive arthropathy may
also develop. The manifestations of gouty arthritis are generally peripheral, in
the hands or feet. Gouty arthritis has a predilection for the joints of the lower
extremity, especially the first MTP joint (podagra), intertarsal joints, ankle, and
knee. The first MTP joint is the most common site of initial involvement; the
great toe is the site of 70% of attacks. Involvement of the hands, wrists, and
elbows may occur later in the clinical course. The limb girdles and axial skeleton
are typically spared. The acute episode usually responds quickly and
dramatically to colchicine or a nonsteroidal antiinflammatory agent such as
indomethacin.
•
FIGURE 19.9 Hydroxyapatite deposition in the acetabular labrum (arrow).
•
FIGURE 19.10 Calcific retrocalcaneal bursitis.
•
FIGURE 19.11 Hydroxyapatite arthropathy. Hip shows destructive changes in the
femoral head and acetabulum. Note the medial acetabular protrusion (protrusio
acetabula, arrow).
METABOLIC DEPOSITION DISEASE

Metabolic deposition diseases involving the joints, in which the body
accumulates a substance it cannot excrete or metabolize, include tophaceous
gout, multicentric reticulohistiocytosis, and amyloidosis. Except for gout, these
types of joint disease are relatively uncommon. If focal, masslike deposits are
located in the musculoskeletal system, the result is a clinically indolent disease
with randomly distributed, slowly enlarging, space-occupying deposits.
Tophaceous Gout
Unlike the other crystal-induced joint conditions, gout may present with the
radiologic features of a metabolic deposition disease.3 Deposits of monosodium
urate crystals are called tophi. The development of tophi requires decades of
sustained hyperuricemia and is related to the degree and duration of
hyperuricemia. Control of hyperuricemia by drugs has reduced the incidence of
tophi in people with gout from more than 50% in the 1950s to approximately 3%
currently. Deposits near the joints and tendons cause a lumpy-bumpy
appearance. These localized areas of swelling may cause the slow development
of pressure erosions on adjacent bone. Such erosions have well-defined sclerotic
margins. A shell of new bone may attempt to encompass the deposit, leaving an
overhanging edge (Figures 19.12–19.15). The articular spaces may be preserved
until late in the disease. Tophaceous gout may occur in combination with
episodes of gouty arthritis.
Dual-energy CT (DECT) relies on the principle that tissues have different
Hounsfield numbers at various kVp (peak kilovoltage). This results in a specific
dual-energy gradient for each material or tissue, which can be used to
characterize biologic tissues or crystals depositions (Figure 19.16). The 2015
American College of Rheumatology and the European League Against
Rheumatism Classification Criteria for Gout included DECT as a criterion for
the diagnosis of gout. The results of DECT studies were found to be helpful for
the differentiation of gout from other inflammatory arthritis, such as psoriatic
and rheumatoid arthritis, and for guiding patient management and improved
clinical outcome in patients with gout.7–9
•
FIGURE 19.12 Tophaceous gout with overhanging edges and chronic erosions of
the first, fourth, and fifth metatarsophalangeal joints. The adjacent articular space in
the first metatarsophalangeal joint is preserved.
•
FIGURE 19.13 Tophaceous gout involving the hand. Posteroanterio radiograph
shows lumpy-bumpy soft-tissue swelling and chronic, focal bone erosions.
•
FIGURE 19.14 Tophaceous gout involving the carpus. Coronal T1 MRI shows
multiple low-signal masses eroding the carpal bones.
•
FIGURE 19.15 Tophaceous gout involving the midfoot. Sagittal CT shows multiple
erosions with fragmentation.
•
FIGURE 19.16 Tophaceous gout. A 3D volume-rendering image of dual-energy CT
of both feet shows extensive deposits of gouty tophi colored in green.
Multicentric Reticulohistiocytosis
In the rare condition of multicentric reticulohistiocytosis, lipid-containing
macrophages are deposited in the soft tissues around joints and tendons in
random distribution. Skin nodules are common. As with gout and other
metabolic deposition diseases, normal bone density and normal joint spaces are
associated with intraosseous and juxta-articular accumulations. Bone erosions
with sclerotic margins and overhanging edges are typical (Figure 19.17), but
sometimes a destructive arthritis ensues (arthritis mutilans). The origin of the
abnormal lipid is unknown. In approximately 28% of cases, multicentric
reticulohistiocytosis seems to be caused by a paraneoplastic disorder related to
an underlying malignancy.
•
FIGURE 19.17 Multicentric reticulohistiocytosis. The soft tissues are thickened, and
there are chronic erosions with overhanging edges.
Amyloid Arthropathy
Amyloidosis is the result of several different underlying diseases in which a
characteristic proteinaceous material accumulates in the body.10 The joint
findings of amyloidosis in chronic renal dialysis patients have been well
documented. Hemodialysis clears beta immunoglobulins poorly from the blood.
As these proteins accumulate in the body, they polymerize into beta-pleated
sheets and become deposited in subcutaneous tissues, around joints, and
occasionally in parenchymal organs. In addition to periarticular masses, a
chronic symmetric arthropathy may also result, with clinical features similar to
those of rheumatoid arthritis. Compression of the median nerve may result from
deposition of amyloid in the carpal tunnel. Contractures and soft-tissue swelling
are common, and severe constitutional symptoms may be present. Amyloidosis
has variable MRI appearance: low T1 and T2 signal (corresponding to fibrous
tissue, amyloid deposits, or both), low T1 and high T2 signal (corresponding to
fluid), and high T1 and T2 signal (corresponding to fatty components) (Figure
19.18).
PIGMENTED VILLONODULAR SYNOVITIS

Pigmented villonodular synovitis (PVNS) is a benign neoplasm (rather than an
inflammatory condition) of the synovium that usually presents as recurrent
monarticular hemorrhagic effusions in adults.11 It may have localized or diffuse
involvement of the joint. The localized variety is typically represented by a focal
nodular mass projecting into a joint. Common locations include the knee or hip,
but any synovial tissue may be involved. Chronic, erosive changes from
thickened, nodular synovial proliferation may be seen on radiographs. Localized
osteoporosis is common. Arthritic changes such as joint space narrowing and
osteophytes are generally absent. Arthrography shows multiple nodular filling
defects (Figure 19.19). MRI shows effusion and multiple low-signal synovial
masses (Figures 19.20 and 19.21). The lesions are pigmented on gross
examination because of hemosiderin deposition from repeated bleeding. On
GRE MRI, the lesions often show blooming artifact due to the hemosiderin
deposition. Enhancement after intravenous gadolinium injection may be seen on
T1 FS MRI.
•
FIGURE 19.18 Amyloid arthropathy. A, Radiograph of the shoulder shows cartilage
space loss and remodeling of the glenohumeral joint. B, Axial GRE MRI shows
synovial masses (arrows) and degenerative changes.
SYNOVIAL CHONDROMATOSIS
Synovial chondromatosis (synovial osteochondromatosis, synovial
chondrometaplasia) is a condition characterized by the presence of multiple,
benign cartilaginous nodules in the synovium. They may be loose within the
joint or attached to the synovium. They may be calcified, ossified, or neither.
When a synovial chondromatosis is not calcified, MRI shows a confluent soft-
tissue mass of high T2 signal within the joint. The mass may have foci of low T1
and T2 signal when there is calcification (Figures 19.22 and 19.23). Synovial
chondromatosis appears to be a reactive process rather than a neoplastic or
degenerative one and can be distinguished histologically from secondary
synovial chondrometaplasia, in which pieces of bone or cartilage from trauma or
osteoarthritis become embedded in the synovium and stimulate a secondary
cartilaginous metaplasia. However, synovial chondromatosis may cause a
mechanical destructive osteoarthritis and coexist with secondary synovial
chondrometaplasia. Men are affected more than women by a ratio of 2:1, and the
peak age of presentation is in the 40s.
•
FIGURE 19.19 Diffuse pigmented villonodular synovitis of the hip. A spot radiograph
of the right hip with intra-articular injection shows multiple nodular filling defects
(arrow).
OSTEOLYSIS OF THE DISTAL CLAVICLE

Osteolysis of the distal clavicle is a painful condition that may result from
repetitive microtrauma or previous acromioclavicular joint trauma.12 On
radiographs, posttraumatic osteolysis is evident as cortical irregularity of the
distal clavicle with cystlike erosions of the subchondral bone, osteopenia, and
soft-tissue swelling (Figure 19.24A). Sometimes, aggressive osteolysis of the
entire distal clavicle may be seen. On MRI, bone marrow edema in the distal
clavicle without marrow edema in the acromion process is characteristic (Figure
19.24B). Soft-tissue swelling, periarticular erosions, and periostitis may also be
present.
SYNOVIAL CYSTS
Small synovial cysts about joints are common. Baker cysts often present as soft-
tissue masses in the popliteal fossa (see chapter 13). Meniscal cysts are another
common type of synovial cyst found about the knee. Meniscal cysts are typically
associated with chronic meniscal tears. Lateral meniscal cysts are most often
found in the anterior aspect of the knee (Figure 19.25), whereas medial meniscal
cysts are typically found in the posterior aspect of the knee. Similar to meniscal
cysts, paralabral cysts may occur at labral tears of the shoulder or hip.
•
FIGURE 19.20 Diffuse pigmented villonodular synovitis of the hip. A, Coronal T1
MRI shows bulky low-signal synovial masses around the left hip with femoral head
erosions. B, Axial GRE MRI shows blooming dark signal around the left hip.
•
FIGURE 19.21 Localized pigmented villonodular synovitis of the knee. A, Sagittal
T1 MRI shows bulky low-signal-intensity mass in the Hoffa fat pad. B, Sagittal T1 FS
Gd MRI shows heterogeneous, strong contrast enhancement (arrow).
FIGURE 19.22 • Synovial chondromatosis of the elbow. Sagittal T1 FS MRI

arthrogram shows synovial chondromas.
•
FIGURE 19.23 Synovial chondromatosis of the shoulder. Oblique sagittal T2 MRI
shows multiple small synovial chondromas filling the subacromial-subdeltoid bursa
(arrow).
FEMOROACETABULAR IMPINGEMENT
Femoroacetabular impingement (FAI) designates a spectrum of developmental
or acquired conditions of the hip in which a morphologic mismatch between the
femoral head and the acetabulum hip may lead to mechanical impingement of
the acetabular rim on the femoral neck at the extremes of motion.13–15 This can
result in restricted range of motion, pain, acetabular labral pathology, and
degenerative changes. Although FAI has been generally divided into 2 distinct
types, based on whether the inciting cause involves the acetabular side (pincer-
type) or the femoral side (cam-type), this breakdown may be artificial, as many
cases reportedly involve both (mixed type). However, it is useful to consider the
2 patterns separately to better understand the pathophysiology, as well as the
imaging findings, of cam- and pincer-type FAI. In the cam type of FAI, the
morphology of the femoral head and neck is abnormal as a result of conditions
such as previous trauma, slipped capital femoral epiphysis, or Legg-Perthes
disease. Cam-type impingement is most commonly seen in young athletic males.
On a radiography of the hip, the normal concavity along the lateral aspect of the
femoral head-neck junction becomes flattened or slightly convex (Figure 19.26).
Traditionally, this has been referred to as the pistol grip deformity. The same
morphologic abnormalities can be seen at CT and MRI.
•
FIGURE 19.24 Osteolysis of the distal clavicle (different patients). A, Radiograph
shows subchondral erosions (arrow). B, Oblique coronal T2 FS MRI shows erosions
and marrow edema (arrow).
•
FIGURE 19.25 Lateral meniscus tear with meniscal cyst. A, Axial T2 FS MRI shows
an ovoid fluid-filled structure adjacent to the anterior horn of the lateral meniscus. B,
Sagittal T2 FS MRI shows horizontal tear in anterior horn of lateral meniscus
associated with a meniscal cyst (arrow).
In the pincer type of FAI, the morphology of the acetabulum is abnormal as a

result of conditions such as acetabular retroversion or protrusio acetabuli.
Patients who may be anatomically predisposed to FAI may be asymptomatic if
they do not engage in activities that require extreme ranges of motion, such as
ballet or yoga. On a properly positioned anteroposterior view of the pelvis, the
anterior rim of the acetabulum should always project medial to the posterior rim
of the acetabulum. In patients with retroversion, the anterior rim of the
acetabulum projects laterally to the posterior rim of the acetabulum. This
typically involves the superior half of the acetabulum. Thus, the edge of the
anterior and posterior rim of the acetabulum crosses over on the anteroposterior
view of the pelvis, the so-called crossover sign (Figure 19.27). On cross-
sectional imaging (CT or MRI), retroversion can be identified if the anterior rim
of the acetabulum is lateral to the posterior rim on the first axial image that
includes the femoral head. Other radiologic features associated with FAI include
synovial herniation pits of the femoral neck (Figure 19.28) and evidence of os
acetabuli (Figure 19.29). MRI can show bony changes associated with FAI and
can detect associated bone marrow edema, which may indicate symptomatic
disease. MRI also detects periarticular pathology that may mimic symptoms of
FAI, including bursitis, tendinous injuries, ischiofemoral impingement, stress
fractures of the femoral neck, and osteonecrosis. Labral injury and articular
cartilage pathology are seen to advantage with direct MR arthrography (Figure
19.30).
•
FIGURE 19.26 Femoroacetabular impingement. Frog lateral radiograph of the left
hip shows loss of concavity and a small bony bump at the femoral head and neck
junction (arrow).
FIGURE 19.27 • Femoroacetabular impingement with a crossover sign.
Anteroposterior (AP) radiograph of the left hip shows the anterior rim of the
acetabulum (white arrow) projects lateral to the posterior rim of the acetabulum (black
arrow). Thus, the edge of the anterior (white line) and posterior (black line) rim of the
acetabulum crosses over on the AP view of the pelvis, the so-called crossover sign.
•
FIGURE 19.28 Synovial herniation pit. Anteroposterior radiograph of the left hip
shows a large synovial herniation pit in the left femoral neck (arrow).
•
FIGURE 19.29 Os acetabula. Anteroposterior radiograph of the left hip shows a
large os acetabuli near the anterior inferior iliac spine (arrow).
SHOULDER IMPINGEMENT
Shoulder impingement is a clinical scenario of painful functional limitation of
the shoulder.16 It is currently subdivided into external and internal impingement.
External causes are due to primary abnormalities in the coracoacromial arch
causing extrinsic compression of the subacromial bursa and the rotator cuff,
leading to rotator cuff tear and retraction, and including subacromial and
subcoracoid impingement. It occurs most commonly in middle-aged nonathletic
individuals. Early theories on etiology focused on anatomical abnormalities of
the coracoacromial arch. However, there is growing evidence that scapular
dysfunction may be more significant, especially in the patient under 40 years of
age. Radiographic and MRI findings of subacromial impingement include a
downward-projecting bony excrescence of acromion, degenerative hypertrophy
of the acromioclavicular joint, subacromial-subdeltoid bursitis, and tendinosis or
tear of the supraspinatus (Figure 19.31).
•
FIGURE 19.30 Cam-type femoroacetabular impingement (FAI) with labral tear.
Radial T1 FS MR arthrogram shows labral tears (arrows) in a patient with a cam-type
FAI (*).
Internal causes of impingement are secondary to rotator cuff and capsular

dysfunction and are categorized by the location of the impingement and the
underlying pathophysiologic or mechanical cause of the impingement. These
include posterosuperior impingement (PSI), anterosuperior impingement,
anterior impingement, and entrapment of the long head of the biceps tendon. PSI
refers to contact of the undersurface of the posterosuperior rotator cuff with the
posterosuperior labrum when the arm is abducted and externally rotated, where
the cuff can become pinched between the labrum and the greater tuberosity. It
occurs most frequently in professional throwing athletes and is attributed to
repetitive overhead motion. The MR findings of PSI include (1) tear of the
posterior undersurface fibers of the supraspinatus tendon and anterior
undersurface of the infraspinatus tendon, (2) tear of the posterosuperior glenoid
labrum, (3) humeral head impaction or subcortical humeral head cysts, (4) laxity
of the anterior capsule, and (5) thickening of the posterior capsule (Figure
19.32).
CUFF TEAR ARTHROPATHY

Rotator cuff tear arthropathy is end-stage degenerative arthropathy of the
shoulder that results from chronic tears of the rotator cuff. Although the exact
pathogenesis is still uncertain, the 3 imaging characteristics of cuff tear
arthropathy are rotator cuff tear, glenohumeral osteoarthropathy, and superior
subluxation of the humeral head.17 The typical rotator cuff tear is massive and
involves the supraspinatus and infraspinatus tendons, resulting in imbalance of
the dynamic stabilizers of the glenohumeral joint. The glenohumeral
osteoarthropathy has typical radiologic features, including asymmetric cartilage
loss, subchondral sclerosis, subchondral cysts, and osteophytes. Chronic superior
subluxation of the humeral head is often associated with erosion and remodeling
of the superior humeral head and the inferior acromioclavicular arch to form a
ball-and-socket articulation in the space formerly occupied by the rotator cuff.
Although radiographs may allow the diagnosis of cuff tear arthropathy (Figure
19.33), MRI is often appropriate for management decisions (Figure 19.34). The
presence and degree of rotator cuff muscle atrophy is an indicator of severity and
chronicity, but some large rotator cuff tears without corresponding muscle
atrophy may be reparable. Cuff tear arthropathy is a common indication for
reverse total shoulder replacement (see chapter 19).
•
FIGURE 19.31 Subacromial impingement. A, Anteroposterior radiograph of the right
shoulder shows subacromial spur (arrow). B, Coronal T2 FS MR arthrogram shows
hypertrophic arthritis involving acromioclavicular joint associated with edema. There is
mild tendinosis of the supraspinatus tendon (arrow).
•
FIGURE 19.32 Posterosuperior impingement of the shoulder. A, Coronal STIR MRI
shows multiple subcortical humeral head cysts. B, Coronal GRE MR arthrogram
shows partial-width, partial-thickness articular-sided tear at the posterior fibers of the
supraspinatus tendon (arrow), associated with a tear of the posterior-superior labrum
(arrowhead).
LIPOMA ARBORESCENS
Lipoma arborescens is a form of chronic synovitis seen primarily in
osteoarthritis of the knee in which there is frondlike fatty proliferation of the
synovium and subsynovial tissues. The appearance is reminiscent of leaves on a
tree with an arborizing pattern, hence the name. On MRI, there is typically a
large joint effusion that outlines the villi, and the villi should follow the signal
characteristics of fat (Figure 19.35). There is no specific clinical significance to
this condition. It may be treated by synovectomy.
•
FIGURE 19.33 Rotator cuff tear arthropathy. Patient with longstanding shoulder
symptoms. Anteroposterior radiograph shows superior subluxation of the humeral
head relative to the glenoid and joint space loss.
•
FIGURE 19.34 Rotator cuff tear arthropathy. A, Coronal PD FS MRI shows superior
subluxation of the humeral head with severe cartilage loss in the glenohumeral joint
and remodeling of the undersurface of the acromion. The supraspinatus and
infraspinatus tendons are absent and presumably torn. There is a large joint effusion
extending into the subdeltoid-subacromial bursa. B, Sagittal PD FS MRI shows
absence of the supraspinatus and infraspinatus tendons, and remodeling of the
undersurface of the acromion. C, Sagittal T1 MRI through the scapula shows
profound fatty atrophy of the supraspinatus and infraspinatus muscles.
•
FIGURE 19.35 Lipoma arborescens. Patient with chronic knee swelling and pain. A,
Sagittal PD FS MRI shows large joint effusion with villous proliferation of the synovium
projecting into the joint space, outlined by the joint fluid. The proliferations have low
signal like fat. B, Coronal T1 MRI shows the fatty synovial proliferations outlined by
low-signal fluid.
References
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osteoarthropathy with and without superimposed osteomyelitis in patients with a diabetic foot. Skeletal
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PMID:26883537].
2. Jones EA, Manaster BJ, May DA, Disler DG. Neuropathic osteoarthropathy: diagnostic dilemmas and
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Rheum Dis Clin North Am. 2016;42(4):621–644. doi:10.1016/j.rdc.2016.07.005 [Epub September 9,
2016. PMID:27742018].
4. Rosenthal AK, Ryan LM. Calcium pyrophosphate deposition disease. N Engl J Med.
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5. Garcia GM, McCord GC, Kumar R. Hydroxyapatite crystal deposition disease. Semin Musculoskelet
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6. Neogi T. Clinical practice. Gout N Engl J Med. 2011;364(5):443–452. doi:10.1056/NEJMcp1001124
[PMID:21288096].
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musculoskeletal imaging (Part 1). Semin Musculoskelet Radiol. 2015;19(5):431–437. doi:10.1055/s-
0035-1569253 [Epub December 22, 2015. PMID:26696081].
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technical approaches, and applications in musculoskeletal imaging (Part 2). Semin Musculoskelet
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PMID:26696082].
9. Fritz J, Henes JC, Fuld MK, Fishman EK, Horger MS. Dual-energy computed tomography of the knee,
ankle, and foot: noninvasive diagnosis of gout and quantification of monosodium urate in tendons and
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14, 2016. PMID:27077593].
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11. Murphey MD, Rhee JH, Lewis RB, Fanburg-Smith JC, Flemming DJ, Walker EA. Pigmented
villonodular synovitis: radiologic-pathologic correlation. RadioGraphics. 2008;28(5):1493–1518.
doi:10.1148/rg.285085134 [PMID:18794322]
12. DeFroda SF, Nacca C, Waryasz GR, Owens BD. Diagnosis and management of distal clavicle
osteolysis. Orthopedics. 2017;40(2):119–124. doi:10.3928/01477447-20161128-03 [Epub December 7,
2016. PMID:27925640].
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PMID:19185661].
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doi:10.2214/AJR.14.13815 [PMID:26496572].
1. Which of the following imaging is most likely to be specific for the diagnosis
of PVNS?
A. T1 FS Gd MRI
B. GRE MRI
C. Dual-energy CT
D. Dual-energy X-ray absorptiometry
2. Atraumatic Lisfranc fracture-dislocation commonly occurs in which
condition?
A. Osteoarthritis
B. Hydroxyapatite deposition disease
C. Systemic lupus erythematosus
D. Neuropathic osteoarthropathy
3. Which radiographic finding in the hand and wrist distinguishes pyrophosphate

arthropathy from osteoarthritis?
A. Osteophytes
B. Periostitis
C. Erosions
4. Which of the following conditions is not typically associated with erosions of

bone?
A. Tophaceous gout
B. Synovial chondromatosis
C. Baker cyst
D. Osteolysis of the distal clavicle

1. B Blooming on GRE MRI is a characteristic feature of PVNS.
2. D Neuropathic osteoarthropathy often affects the Lisfranc joints.
3. D Chondrocalcinosis is a radiographic hallmark of CPPD deposition disease
and its more advanced form, pyrophosphate arthropathy. Osteophytes are
common in both osteoarthritis and pyrophosphate arthropathy, but periostitis and
erosions are generally found in neither.
4. C Baker cyst is not specifically associated with erosions of bone.
20
Imaging of Nontraumatic Foot
Conditions
Felix S. Chew
This chapter describes many nontraumatic conditions that are unique to the foot.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of foot conditions in adults, the
4. summarize relevant concepts and knowledge for the following topics: acquired flatfoot, diabetic
foot, corrected clubfoot, tarsal coalition, Haglund deformity, plantar fasciitis, sinus tarsi
syndrome, talar dome osteochondral defect, accessory navicular syndrome, sesamoiditis,
bunion deformity, hallux rigidus, Freiberg disease, Morton neuroma, lesser toe deformities, and
frostbite.
FOOT ANATOMY AND BIOMECHANICS

The bones of the foot are typically divided into the hindfoot, consisting of the
talus and calcaneus; the midfoot, consisting of the navicular, cuboid, and medial,
middle, and lateral cuneiforms; and the forefoot, consisting of the metatarsals
and the phalanges of the toes. The bones of the hindfoot and midfoot are tarsal
bones. The articulation between the hindfoot and midfoot is the Chopart joint
(talonavicular and calcaneocuboid joints) and the articulation between the
midfoot and forefoot is the Lisfranc joint (tarsal-metatarsal joints). The
articulation between the talus and the calcaneus is the subtalar joint and consists
of posterior, middle, and anterior facets. The posterior facet is large and roughly
rectangular in shape. The middle facet is at the superior surface of the
sustentaculum tali, and the anterior facet, the smallest, extends to the anterior
process. The rounded head of the talus resembles the head of the femur, and the
socket that it fits into is called the acetabulum pedis. The acetabulum pedis is
formed by the articular surfaces of the navicular and anterior and middle subtalar
facets and by various supporting ligaments, particularly the spring ligament
complex. The spring (plantar calcaneonavicular) ligament complex attaches the
inferior margins of the navicular to the anterior margin of the sustentaculum tali.
The foot may also be divided into a medial column, consisting of the talus,
navicular, cuneiforms, and first 3 metatarsals and toes, and a lateral column,
consisting of the calcaneus, cuboid, and fourth and fifth metatarsals and toes.
There are 3 arches of the foot, the lateral and medial longitudinal arches and
the transverse arch. The lateral longitudinal arch consists of the bones along the
lateral side of the foot (calcaneus, cuboid, and fifth metatarsal). The medial
longitudinal arch consists of the bones along the medial side of the foot
(calcaneus, talus, navicular, first cuneiform, first metatarsal). The plantar
aponeurosis, the long and short plantar (inferior calcaneocuboid) ligaments, and
the spring ligament complex together function as bowstrings to help maintain the
longitudinal arches. The tibialis posterior tendon is the primary dynamic
stabilizer of the medial arch and is near the superior medial oblique portion of
the spring ligament. The transverse arch extends through the midfoot and
metatarsal bases.
Motion and alignment of the foot depend on positioning and stress and vary
throughout the gait. Non-weight-bearing radiographs are unreliable for
determining foot alignment. The following discussion of foot alignment assumes
weight-bearing anteroposterior (AP) and lateral foot radiographs. On both AP
and lateral radiographs of the feet with normal alignment, the axis of the talus
should pass straight through the axes of the navicular, medial cuneiform, and
first metatarsal (Figure 20.1) and the navicular should cover the articular surface
of the head of the talus symmetrically. The axis of the calcaneus should pass
between the fourth and fifth metatarsals on the AP radiograph. There are many
methods of measurement involving the alignment of the foot, some of which
may be useful (Figure 20.2).1,2
ACQUIRED FLATFOOT
Flatfoot (pes planus alignment) is most often hereditary and asymptomatic.
Acquired flatfoot in adults is a symptomatic condition in which the medial
longitudinal arch collapses during standing. As much as 7% to 10% of the adult
population may be affected, and it is particularly common in women older than
50 years. The tibialis posterior muscle is the major dynamic stabilizer of the
medial arch and inserts at the medial aspect of its keystone, the navicular, as well
as along the second cuneiform and metatarsals. Tibialis posterior tendon
dysfunction, usually from cumulative wear and tear, coupled with degenerative
attrition of the spring ligament complex, is the most common cause of acquired
adult flatfoot.3–5 As the tendon fails, the medial arch progressively flattens,
leading to a cascade of secondary abnormalities, including hindfoot valgus,
forefoot supination, and forefoot abduction (pes planovalgus). In early stages,
with the onset of peritendinitis and tendinopathy, flexible flatfoot develops. In
late stages, with complete rupture of the tibialis posterior tendon, rigid flatfoot
develops followed by lateral peritalar subluxation, hindfoot valgus, and collapse
of all 3 arches.
•
FIGURE 20.1 Normal foot. Normal foot in which the axes of the talus, navicular,
medial cuneiform, and first metatarsal are collinear (talar-first metatarsal angle = 0°)
and the navicular covers the head of the talus symmetrically on both anteroposterior
(AP) and lateral views. A, AP view. B, Lateral view.
On the weight-bearing lateral radiograph, the talus, navicular, first cuneiform,

and first metatarsal should be oriented in a straight line (Figure 20.1B). If the
midfoot is convex dorsally, cavus alignment is present (Figure 20.3A). Pes
planus alignment is characterized by sagging of the midfoot below this
hypothetical line at either the talonavicular joint or the navicular-cuneiform joint
(Figure 20.3B), indicating loss of the medial arch. Additional features of flatfoot
include an increased plantar gap at the first tarsometatarsal (TMT) and
calcaneocuboid joints; normally, these articular surfaces are parallel on the
lateral view. Lateral peritalar subluxation is another common component of
acquired flatfoot in which a planovalgus deformity is present and may be seen
on AP radiographs as asymmetric coverage of the head of the talus by the
navicular (Figure 20.4; compare with Figure 20.1). Hindfoot valgus may be
recognized on the lateral view by an increase in the lateral calcaneal angle. An
additional radiologic feature of flatfoot may be superimposition of the metatarsal
bases, indicating loss of the transverse arch. On the weight-bearing AP
radiograph, the metatarsals may appear splayed and the talocalcaneal angle may
be widened.
Surgical treatment of acquired flatfoot includes stabilization of the medial
column, lengthening of the lateral column, and medialization of the heel (varus
osteotomy of the calcaneus) (Figure 20.5).
DIABETIC FOOT
We frequently recognize diabetes on foot radiographs from calcification of the
interdigital arteries, a finding that is very common in diabetics but otherwise
uncommon (Figure 20.6).
The diabetic foot is an unfortunate confluence of diabetic morbidities
affecting the foot.6–8 Chronic ulceration and infection are the result of peripheral
neuropathy and vascular insufficiency. Sensory loss leads to unrecognized
trauma, often minor but chronic and repetitive. Motor defects result in foot
deformities that lead to pressure points and unusual weight-bearing areas where
the skin breaks down and chronic ulcers form. Gradual derangement of the
normal foot architecture progresses in a vicious cycle of progressive deformity
(Figures 20.7 and 20.8).
•
FIGURE 20.2 Lateral foot alignment. A, Calcaneal pitch angle: Lateral view, tangent
along inferior surface of calcaneus and a line from the inferior surface of the calcaneal
tuberosity to the inferior surface of the fifth metatarsal base (normal 20-30°). B, Talar
base (declination) angle is the axis of the talus versus the floor (normal 14-36°). C,
Lateral talocalcaneal (kite) angle: Lateral view, calcaneal tangent versus long axis of
the talus (normal 25-45°). Increased is hindfoot valgus.
Autonomic deficits and vascular disease contribute to impaired host defenses

against infection. Pedal osteomyelitis results almost exclusively from contiguous
infections and occurs most frequently around the fifth and first
metatarsophalangeal (MTP) joints.9 Osteomyelitis usually occurs directly
adjacent to skin ulcers or surgical defects. Spread of osteomyelitis to adjacent
bones may then occur. Imaging has a particular role in the diagnosis of
infections. At the University of Washington, we begin with radiographs and
quickly move on to MRI (Figure 20.9). Although we prefer to use MRI with
gadolinium enhancement when searching for infection, our current guideline is
that diabetics generally should not receive gadolinium if their estimated
glomerular filtration rate is below 30. The typical radiographic findings of
osteomyelitis may be absent in the diabetic foot because the blood supply is
often inadequate for reactive bone formation and osteoporosis. Distinguishing
infection from neuropathic osteoarthropathy is a particular challenge that may
require needle aspiration or bone biopsy to resolve. However, our experience
suggests that infections typically affect the forefoot and heel, and neuropathic
osteoarthropathy typically affects the midfoot and Lisfranc joints.
•
FIGURE 20.3 Foot alignment on weight-bearing lateral radiographs. A, Cavus foot
with a dorsally convex midfoot. B, Flatfoot with sagging between the navicular and
medial cuneiform results in a dorsally concave midfoot.
FIGURE 20.4 • Severe pes planovalgus. A, Anteroposterior weight-bearing
radiograph shows lateral peritalar subluxation. B, Lateral weight-bearing radiograph
shows decreased calcaneal pitch angle, indicating flattening of the lateral longitudinal
arch. The midfoot is dorsally concave, indicating flattening of the medial longitudinal
arch. The metatarsals are superimposed on each other, indicating flattening of the
transverse arch.
•
FIGURE 20.5 Treatment of acquired flatfoot. A and B, Anteroposterior and lateral
radiographs of lateral column lengthening with insertion of metal foam wedge, medial
column stabilization with first tarsometatarsal arthrodesis, and medializing internally
fixed calcaneal osteotomy. C, Intraoperative axial radiograph of the calcaneus shows
the medial displacement osteotomy has been fixed by specialized hardware.
•
FIGURE 20.6 Diabetic foot with multiple interdigital arterial calcifications.
•
FIGURE 20.7 Early diabetic neuropathic osteoarthropathy. A, Anteroposterior
radiograph shows displaced fracture fragment from medial cuneiform. There is lateral
subluxation of the 3 cuneiforms relative to the navicular. B, Lateral radiograph shows
soft-tissue swelling, but the arch of the foot is maintained.
FIGURE 20.8 • Late diabetic neuropathic osteoarthropathy. A, Anteroposterior

radiograph shows severe fragmentation of the cuneiforms, navicular, and cuboid. The
naviculocuneiform and Chopart joints are completely disorganized, and there is lateral
subluxation of the tarsometatarsal joints. B, Lateral radiograph shows complete
collapse of the midfoot with the metatarsals overriding the talus and midfoot
fragments. The arch is now in rocker-bottom alignment.
Surgical reconstruction of the diabetic foot typically requires extensive

fusions of the hindfoot, midfoot, and sometimes TMT joints (Figure 20.10).
Realignment of the bones to eliminate pressure points may allow chronic ulcers
to heal. A robust blood supply is necessary for healing, and the presence of
infection is a contraindication.
CORRECTED CLUBFOOT
Clubfoot (talipes equinovarus) is a congenital condition that is often diagnosed
in utero and is typically treated in infancy by serial casting. Occasionally, one or
more operations are needed. Adults with corrected clubfoot may present with
residual deformities, secondary degenerative arthritis, tendinosis, stress
fractures, and gait disturbance, among other problems.10 On radiographs,
corrected clubfoot in adults may often be recognized as unilateral cavovarus
alignment.
•
FIGURE 20.9 Diabetic neuropathic osteoarthropathy. A, Sagittal T1 MRI shows
dorsal subluxation of the midfoot with fragmentation of tarsal bones (arrow). B,
Sagittal T2 FS MRI shows edema in the bones involved with the neuropathic joint, as
well as in the adjacent soft tissues. A plantar ulceration is present with adjacent
inflammatory change (arrow).
•
FIGURE 20.10 A and B, Anteroposterior and lateral radiographs of Charcot foot
reconstruction with fusions of the hindfoot, midfoot, and first tarsometatarsal joints.
TARSAL COALITION
Tarsal coalition is an abnormal articulation between tarsal bones that results from
lack of segmentation rather than from ankylosis. Most coalitions are
calcaneonavicular or subtalar and bilateral in about 20%. A coalition restricts
foot mobility, typically presenting as a painful flatfoot in adolescence as the
skeleton matures. Adults may complain of pain from secondary osteoarthritis.11
Radiographs should be obtained initially, but CT and MRI are excellent methods
for diagnosing tarsal coalitions and evaluating secondary degenerative changes.
An indirect sign of a coalition between the calcaneus and the talus is talar
beaking, a spur from the anterior superior aspect of the talus resulting from
abnormal talonavicular motion. The C-sign may be evident on lateral views
when a middle facet coalition is present. The dome of the talus forms the top of
the C, the coalition forms the middle, and the sustentaculum forms the bottom
(Figure 20.11). On CT or MRI, continuity of cortex and marrow space across the
expected location of an intertarsal joint indicates a bony coalition (Figure 20.12).
HAGLUND DEFORMITY
Haglund deformity is a prominence of the posterior superior margin of the
calcaneus that becomes symptomatic because of impingement of improperly
fitted footwear. The bony deformity may lead to a mechanically induced
inflammation of the superficial bursa, Achilles tendinosis, and retrocalcaneal
bursitis.12 These symptomatic inflammatory changes in the presence of the bony
deformity, often visualized on radiography and MRI, are together known as
Haglund syndrome (Figure 20.13). The surgical treatment includes excision of
the bony prominence and debridement of the Achilles tendon (Figure 20.14).
•
FIGURE 20.11 Adult presentation of tarsal coalition. A and B, Lateral radiographs of
the right and left feet show bilateral talar beaks (arrow) and C-signs (short arrows).
There is bilateral pes planus with decreased calcaneal pitch angles.
•
FIGURE 20.12 Incidental tarsal coalition in adult with calcaneal stress fracture from
running. A, Axial T1 MRI shows bony bridge across the usual location of the middle
subtalar facet (arrow). B, Coronal PD FS MRI shows the bony bridge (arrow). The
marrow edema is the result of the stress fracture (not shown).
PLANTAR FASCIITIS AND HEEL FAT PAD SYNDROME

Plantar fasciitis is a common chronic overuse injury of the plantar aponeurosis,
usually the origin of the central cord at the medial calcaneal tuberosity, which
presents as a subcalcaneal heel pain. It is related to weight-bearing activities,
obesity, improper shoes, and foot deformities and is typically self-limited. On
MRI, the plantar aponeurosis may be thickened at its origin and show increased
T2 signal.13 Surrounding edema may also be present in the soft tissues and
occasionally in the adjacent calcaneal tuberosity (Figure 20.15). The presence or
absence of a plantar calcaneal enthesophyte is apparently not relevant. Tears of
the plantar aponeurosis are uncommon.
•
FIGURE 20.13 Haglund syndrome. Sagittal STIR MRI shows prominent posterior
calcaneal process (arrow) associated with insertional tendinosis of the Achilles tendon
and retrocalcaneal bursitis.
•
FIGURE 20.14 Haglund syndrome. A, Preoperative lateral radiograph shows bony
prominence of the dorsal calcaneus (arrow) and soft-tissue edema in the Kager fat
pad (short arrow). B, Postoperative radiograph shows resection of the bony
prominence and debridement of the Achilles tendon.
•
FIGURE 20.15 Plantar fasciitis. Sagittal T2 FS MRI shows high signal at the
calcaneal origin of the central cord of the plantar aponeurosis (arrow).
Heel fat pad syndrome may present with symptoms similar to plantar fasciitis
but is related to the heel fat pad that is superficial to the calcaneal tuberosity and
plantar fascia. Overuse, trauma, excessive weight, or loss of fat pad elasticity
may contribute to pain. Radiographs are typically normal, but MRI may show
edema within the heel fat pad (Figure 20.16).13
SINUS TARSI SYNDROME

The sinus tarsi is the space between the neck of the talus and the calcaneus and
contains the interosseous talocalcaneal ligament and fat. Sinus tarsi syndrome is
a clinical condition of pain and subtalar joint instability caused by ligamentous
injuries, possibly chronic or athletic. Scarring and inflammation may be
demonstrated on MRI (Figure 20.17), and symptoms may be alleviated by
injection of steroids into the sinus tarsi or surgery to reduce instability.
•
FIGURE 20.16 Heel fat pad syndrome. Athlete with heel pain after switching to
different shoes. A, Sagittal T1 MRI shows ill-defined low signal in the heel pad
overlying normal plantar fascia. B, Sagittal PD FS MRI shows edema in the heel pad.
•
FIGURE 20.17 Sinus tarsi syndrome. Basketball injury resulted in chronic and
recurrent pain. A, Sagittal PD FS MRI shows edema in the sinus tarsi and the anterior
calcaneus. The normal interosseous talocalcaneal ligament is not seen. B, Sagittal T1
MRI shows loss of the normal bright fat signal in the sinus tarsi.
TALAR DOME OSTEOCHONDRAL DEFECT

The terms “osteochondral defect” and “osteochondritis dissecans” (also OCD)
are often applied to traumatic osteochondral fractures of the talar dome.
Associated osteochondral injuries of the fibula or tibial plafond may occur.
Patients usually present with ankle pain and are evaluated by radiography and
often MRI or CT (see Figure 10.16). Osteonecrosis of attached and detached
fragments is common. If displaced, the fragment becomes a loose body within
the joint capsule. There is a diversity of surgical treatments, including
debridement, excision, curettage, drilling, bone marrow stimulation, bone
grafting (Figure 20.18), and prosthetic replacement.14
ACCESSORY NAVICULAR SYNDROME

The accessory navicular bone is a common accessory bone located at the
proximal medial aspect of the navicular. There are 3 commonly recognized types
of accessory navicular bones: Type 1 is a small ovoid ossicle contained within
the tibialis posterior tendon; Type 2 is a larger unfused secondary ossification
center articulating with the navicular by a synchondrosis; and Type 3 is a
medially prominent cornuate navicular that probably represents fusion of Type 2.
Type 1 accessory navicular bones are typically asymptomatic. Type 2 accessory
navicular bones may receive a portion of the tibialis posterior insertion and
become symptomatic from chronic repetitive stress on the synchondrosis
(accessory navicular syndrome). In this situation, MRI may show marrow edema
in the accessory navicular bone (Figure 20.19) or in the subchondral bone on
both sides of the synchondrosis.15 Type 3 accessory navicular bones may cause
symptoms from the bony prominence but typically not from the posterior tibialis
tendon insertion.
•
FIGURE 20.18 Talar dome osteochondral defect. A, Coronal T1 MRI shows low
signal in the medial half of the talar dome. B, Coronal STIR MRI shows marrow
edema corresponding to the abnormal region. The tibial side of the joint is normal. C
and D, Postsurgical anteroposterior and lateral radiographs show osteochondral
allograft replacement of the affected portion of the talar dome, with internal fixation.
•
FIGURE 20.19 Accessory navicular syndrome in a patient with medial midfoot pain.
A, Axial T1 MRI shows an accessory navicular (Type 2) (arrow). B, Axial PD FS MRI
at the same anatomic level shows marrow edema within the accessory navicular
(arrow) and high signal in the distal tibialis posterior tendon (short arrow).
SESAMOIDITIS
Sesamoiditis refers to pain of the sesamoids of the great toe and their
surrounding tissues, usually because of chronic repetitive trauma or overuse. As
such, it may not represent an actual inflammatory process but rather a stress
reaction or stress fracture. Because their blood supply is typically a single
proximal vessel, the sesamoids are also vulnerable to osteonecrosis. Patients
complain of pain underneath the ball of the foot, and radiography may be normal
or show fracture or sclerosis of the involved sesamoid. MRI may show T2 bright
edema in the sesamoid and thickening of the surrounding soft tissues (Figure
20.20).16 Radionuclide bone scan will show abnormal activity in the sesamoid.
Sometimes, an actual fracture may be demonstrated on imaging. Treatment is
typically conservative, similar to treatment for stress fracture or tendinitis
elsewhere in the body. Occasionally, the painful sesamoid is surgically excised
(sesamoidectomy). An important differential diagnosis is osteoarthritis between
the sesamoids and the head of the first metatarsal.
BUNION DEFORMITY
A bunion (hallux valgus, metatarsus primus varus) is a symptomatic complex of
deformities characterized by a bony prominence at the medial aspect of the first
MTP joint. It consists of lateral deviation of the great toe (hallux valgus), medial
deviation of the first metatarsal (metatarsus primus varus), soft-tissue
contractures of the great toe flexors, and secondary degenerative change at the
first MTP joint.17 Progressive soft-tissue contracture pulls like a bowstring to
increase the deformity. A bunion can be recognized on weight-bearing AP
radiographs of the foot by varus deviation of the first metatarsal and valgus
deviation of the great toe (Figure 20.21). The degree of uncovering of the
articular surface of the first metatarsal head by the proximal phalanx of the great
toe depends on the severity of the hallux valgus. Together, these deformities
result in lateral subluxation of the sesamoids relative to the head of the first
metatarsal. Second MTP and toe deformities commonly accompany bunions. In
severe cases, the second toe may override the deviated great toe. Many
operations have been devised to treat bunions. The modified Lapidus operation
corrects the underlying first metatarsal varus deformity and fuses the first TMT
joint (Figure 20.22). The first metatarsal prominence may also be reduced and
the alignment of the great toe may be corrected. Other operations may shorten
the first metatarsal and move the metatarsal head laterally to ameliorate the
bowstring effect (Figure 20.23).
•
FIGURE 20.20 Sesamoiditis. Patient presented with chronic activity-related pain
under the medial side of the ball of the foot. A, Short-axis PD FS MRI shows
abnormal high signal in the medial sesamoid (arrow), corresponding to the external
marker (arrowhead). The lateral sesamoid (long arrow) is normal. B, Sagittal PD FS
MRI through the lateral sesamoid shows it to be normal. C, Sagittal PD FS MRI
through the medial sesamoid shows abnormal high signal. D, Long-axis T2 FS shows
abnormal high signal in the medial sesamoid surrounding a transverse nondisplaced
fracture (arrow).
HALLUX RIGIDUS
Hallux rigidus is a common degenerative condition involving the great toe in
which osteoarthritis with osteophyte formation results in pain and loss of range
of motion in dorsiflexion at the first MTP joint. Typically, a dorsal osteophyte at
the head of the first metatarsal may be recognized on lateral radiographs (Figure
20.24). The loss of first MTP dorsiflexion affects the terminal stance and
preswing portions of the gait, and high-heeled shoes that keep the toes in
dorsiflexion may be difficult to wear. Surgical treatments include cheilectomy
(resection of the dorsal osteophyte), arthrodesis, and joint replacement.18,19
FREIBERG DISEASE
Freiberg disease (Freiberg infraction) is a symptomatic collapse of the articular
surface of the metatarsal, usually the second, that appears to be the result of
altered biomechanics, vascular compromise, and genetic predisposition.20 Onset
is most common in young women, but degenerative sequelae persist in older
adults. Radiographically, it may be recognized as flattening of the subchondral
bone of the distal metatarsal (Figure 20.25). If the disease progresses, collapse,
fragmentation, and secondary degenerative changes may follow.
•
FIGURE 20.21 Bunion deformity (hallux valgus, metatarsus primus varus). A,
Anteroposterior weight-bearing radiograph of the foot shows varus deformity of the
first metatarsal combined with valgus deformity of the great toe. Note the overriding of
the second toe over the great toe and lateral subluxation of the lateral sesamoid
(arrow), relative to the head of the first metatarsal. B, Short-axis T1 MRI through the
head of the first metatarsal shows lateral subluxation of the sesamoids (arrow) with
degenerative change.
FIGURE 20.22 • Bunion correction. A, Preoperative bunion deformity. B,
Postoperative modified Lapidus procedure with proximal phalanx osteotomy (Akin
procedure).
MORTON NEUROMA
Morton neuroma is a nonneoplastic thickening of the soft tissues around the
digital nerve as it passes the intermetatarsal ligament at the metatarsal heads,
most often between the third and fourth toes. Repetitive trauma, ischemia,
entrapment, and tethering have been postulated as causes of Morton neuroma,
and histology shows perineural fibrosis.21 The typical patient complains of sharp
burning forefoot pain in the characteristic location, and the diagnosis is made
clinically; MRI or sonography may sometimes confirm the presence of the
lesion. There are no radiographic features of Morton neuroma. MRI may show
an interdigital mass at the plantar aspect between the involved metatarsal heads
with low or intermediate T1 and T2 signals and often intense enhancement with
gadolinium (Figure 20.26). Sonography may show a hypoechoic mass in the
appropriate location.
•
FIGURE 20.23 Bunion correction with shortening and displacement osteotomy of
the first metatarsal, fixed by K-wire. Also note reshaping of the medial aspect of the
foot by resection of the bony protuberances of the proximal phalanx and first
metatarsal.
LESSER TOE DEFORMITIES

Deformities of the lesser toes are usually caused by imbalances of the intrinsic
and extrinsic muscles of the foot. A hammertoe deformity is flexion at the
proximal interphalangeal (PIP) joint, usually with extension at the distal
interphalangeal (DIP) joint and neutral or extension at the MTP joint (Figures
20.27 and 20.28). A mallet toe deformity is DIP flexion with PIP and MTP joints
in neutral. A claw toe deformity is hyperextension of the MTP joint and flexion
of the PIP and DIP joints. A crossover toe is associated with MTP instability. It is
typically seen where the second toe crosses over a severe hallux valgus. When
conservative measures fail, these toe deformities may be treated surgically with
resection arthroplasty or arthrodesis.22 Tendon transfers or metatarsal
osteotomies may also be performed. A bunionette deformity is a bony
prominence on the lateral side of the fifth metatarsal head. When symptomatic,
there may be overlying soft-tissue swelling, similar to a bunion. Corrective
osteotomy of the prominence may ameliorate the symptoms.
COLD INJURIES
Cold injuries are essentially vascular injuries.23 In chilblains or immersion foot,
prolonged exposure to low but nonfreezing temperatures causes vasoconstriction
and hypoxic damage. Leakage of physiologic fluids from damaged small vessels
leads to pain and edema. An intense hyperemic and inflammatory response
develops; this is usually painful and often lasts for days to weeks. Ultimate
recovery is common, but the affected part typically remains more sensitive to
cold than before the exposure. Damp cold has a greater effect than cold at low
humidity.
•
FIGURE 20.24 Hallux rigidus. A, Oblique foot radiograph shows a prominent dorsal
osteophyte at the first metatarsophalangeal joint. B, Postsurgical foot radiograph
shows the bony prominence has been smoothed.
FIGURE 20.25 • Freiberg infraction of the second metatarsal head. A,

Anteroposterior foot radiograph shows sclerosis. B, Oblique foot radiograph shows
osteochondral collapse (arrow).
•
FIGURE 20.26 Morton neuroma. A, Short-axis PD FS MRI through the forefoot
shows poorly marginated high signal (arrow) between the second and third metatarsal
heads, corresponding to the site of discomfort. B, Long-axis PD FS MRI shows the
edema (arrow) in the plantar soft tissues.
•
FIGURE 20.27 Hammertoes. A and B, Anteroposterior and lateral radiographs
show proximal interphalangeal joint flexion deformities of the lesser toes.
•
FIGURE 20.28 Second toe hammertoe shown on sagittal T1 MRI.
In freezing injuries or frostbite—to which the toes are particularly vulnerable
—the formation of ice crystals within the tissues may cause permanent damage.
On radiographs, one may initially see soft-tissue edema, then osteoporosis, and
periostitis. Soft tissue and even bone loss from tuftal resorption may become
evident over a period of weeks, and a demarcation between viable and necrotic
tissues may be visible (Figure 20.29). Autoamputation of soft tissue and bone
may be the ultimate result. Cartilage damage may result in secondary
degenerative joint disease. Acute evaluation of cold injuries may include
arteriography or radionuclide perfusion studies. MRI with gadolinium may show
the demarcation between perfused and nonperfused tissues.
•
FIGURE 20.29 Frostbite. A, Anteroposterior radiograph of the right toes obtained
6 weeks after cold injury shows diminution of the distal soft tissues of the first,
second, and third toes. B to D, Sagittal T1 FS Gd MRI of the first (B), second (C), and
third (D) toes shows low signal in the infarcted distal soft tissues and enhancement
throughout the remaining tissues; the fourth toe (E) is intact and enhances.
References
1. Thapa MM, Pruthi S, Chew FS. Radiographic assessment of pediatric foot alignment: review. AJR Am J
Roentgenol. 2010;194(6 suppl):S51–S58. doi:10.2214/AJR.07.7143 [PMID:20489117].
2. Lin YC, Mhuircheartaigh JN, Lamb J, Kung JW, Yablon CM, Wu JS. Imaging of adult flatfoot:
correlation of radiographic measurements with MRI. AJR Am J Roentgenol. 2015;204(2):354–359.
doi:10.2214/AJR.14.12645 [PMID:25615758].
3. Yao K, Yang TX, Yew WP. Posterior tibialis tendon dysfunction: overview of evaluation and
management. Orthopedics. 2015;38(6):385–391. doi:10.3928/01477447-20150603-06
[PMID:26091214].
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and findings in acquired adult flatfoot deformity. Semin Musculoskelet Radiol. 2016;20(1):104–115.
doi:10.1055/s-0036-1580616 [Epub April 14, 2016. PMID:27077591].
6. Peters EJ, Lipsky BA. Diagnosis and management of infection in the diabetic foot. Med Clin North Am.
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7. Glaudemans AW, Uçkay I, Lipsky BA. Challenges in diagnosing infection in the diabetic foot. Diabet
Med. 2015;32(6):748–759.
8. Ergen FB, Sanverdi SE, Oznur A. Charcot foot in diabetes and an update on imaging. Diabet Foot
Ankle. 2013;4:10.
9. Ledermann HP, Morrison WB, Schweitzer ME. MR image analysis of pedal osteomyelitis: distribution,
patterns of spread, and frequency of associated ulceration and septic arthritis. Radiology.
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doi:10.1016/j.fcl.2010.03.002 [PMID:20534356].
11. Flynn JF, Wukich DK, Conti SF, Hasselman CT, Hogan MV, Kline AJ. Subtalar coalitions in the adult.
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12. Vaishya R, Agarwal AK, Azizi AT, Vijay V. Haglund’s syndrome: a commonly seen mysterious
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13. Chang CD, Wu JS. MR imaging findings in heel pain. Magn Reson Imaging Clin N Am. 2017;25(1):79–
93. doi:10.1016/j.mric.2016.08.011 [PMID:27888853].
14. Hannon CP, Smyth NA, Murawski CD, et al. Osteochondral lesions of the talus: aspects of current
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[PMID:24493179].
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21. Kay D, Bennett GL. Morton’s neuroma. Foot Ankle Clin. 2003;8(1):49–59 [PMID:12760574].
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1. Lateral peritalar subluxation on AP weight-bearing foot radiographs is a sign

of which alignment deformity?
A. Pes planus
B. Pes cavus
C. Pes planovalgus
D. Pes cavovarus
2. Which radiographic finding on foot radiographs suggests that the patient is

diabetic?
A. Tarsal coalition
B. Pes cavovarus alignment
D. Interdigital arterial calcification
3. Which condition typically involves the calcaneus?

A. Freiberg disease
B. Morton neuroma
C. Haglund disease
D. Accessory navicular syndrome
4. Acquired flatfoot in adults is most closely associated with abnormality of

which tendon?
A. Tibialis posterior
B. Flexor hallucis longus
C. Extensor digitorum longus
D. Peroneus brevis

1. C Lateral peritalar subluxation occurs with pes planovalgus.
2. D Interdigital arterial calcification in the foot is characteristic of diabetes.
3. C Haglund disease involves the calcaneus.
4. A Tibialis posterior dysfunction is associated with acquired flatfoot.
21
Imaging of the Postsurgical Lower
Extremity
This chapter discusses the postsurgical radiology of common operations of the

lower extremity.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of the postsurgical lower extremity,
4. summarize relevant concepts and knowledge for the following topics: hip osteotomy, femoral
head core decompression, hip arthrodesis, hip arthroplasty, joint replacement materials, hip
replacement, knee extensor realignment, knee replacement, ankle arthrodesis, ankle
replacement, and tumor reconstruction.
HIP SURGERY
Osteotomy
An osteotomy is an operation that involves a surgical cut through the bone.1,2
Osteotomies are commonly performed to change the alignment, length, or shape
of a bone. For example, a fracture malunion with angular deformity may be
revised by an osteotomy that realigns the fragments. Osteotomies may be
described by their site and the direction of change in the distal fragment. A
valgus osteotomy of a long bone realigns the distal fragment into valgus relative
to its original alignment. A lateral displacement osteotomy repositions the distal
fragment laterally. Shortening is accomplished by the removal of bone.
Lengthening may be accomplished by displacement of overlapping fragments by
the insertion of bone graft or by bone distraction using an external fixator.
Osteotomies are also used to alter the alignment and biomechanics of joints.
Angular or rotational osteotomies of the proximal femur alter the major weight-
bearing portion of the femoral head in the treatment of hip dysplasia, early
osteoarthritis, or similar conditions (Figure 21.1). An innominate osteotomy may
be used to deepen the acetabulum and provide better coverage for the femoral
head (Figure 21.2). The fixation techniques and healing of osteotomies are
similar to those of fractures, and the hardware devices used to treat fractures are
applicable (see chapter 4). Complications of healing are rare.
Changes in rotational alignment may also be made; these are called rotational
osteotomies. CT is used for assessment of limb rotation (Figure 21.3). Femoral
version refers to the angle in the axial plane between the femoral neck and the
femoral condyles. Femoral anteversion (the femoral neck is externally rotated
relative to the knee) of approximately 8° in men and 14° in women is average.
Tibial torsion refers to the angle in the axial plane between the ankle mortise and
the tibial condyles. External tibial torsion (the ankle is externally rotated relative
to the knee) of approximately 29° is average. In adults, acquired limb rotation
abnormalities are usually the result of malunion following femoral shaft or tibial
shaft fractures, and rotational osteotomies may be performed to correct them
(Figure 21.4). In unilateral posttraumatic torsional deformities, it is the
difference between right and left in femoral anteversion or tibial torsion that is
clinically important.
Core Decompression
Osteonecrosis of the femoral head is treated surgically. Because the
pathophysiology is thought to be related to increased intraosseous pressure
within the femoral head and neck resulting in ischemia, core decompression to
relieve the pressure may be performed, sometimes in conjunction with
vascularized fibular autograft (Figure 21.5) or other implants to promote the
bone repair process. However, once subchondral collapse occurs, the hip will
ultimately progress to end-stage secondary osteoarthrosis.
Arthrodesis
An arthrodesis is a surgical fusion of a joint.1,2 An intra-articular arthrodesis is
accomplished by resecting the joint and fixing the ends of the articulating bones
together. Internal or external fixation may be used as well as bone graft. A healed
and remodeled arthrodesis has a continuous cortex and trabecular structure
across the site (Figure 21.6). Adaptive changes may occur in adjacent joints in
response to the loss of motion. Joint pain in arthritis can be eliminated by
synovectomy and arthrodesis. Because there are functionally better alternatives,
arthrodesis is uncommonly used at the hip.
•
FIGURE 21.1 Valgus osteotomy of the proximal femur. A, Anteroposterior (AP)
radiograph of the hip at 6 weeks after percutaneous screw fixation for femoral neck
fracture shows impaction of the fracture. The compression screws have backed out
through the lateral cortex as the head has settled further into the neck. B, AP
radiograph after valgus osteotomy of the proximal femur and internal fixation by blade
plate.
•
FIGURE 21.2 Innominate osteotomy for Legg-Perthes disease in a young adult.
The entire acetabulum was mobilized, rotated to cover the femoral head, and
internally fixed. A, Anteroposterior radiograph. B, Steep oblique radiograph.
When joint disease progresses to its end stage, disabling pain and/or
functional limitations may be treated surgically. An arthroplasty is a surgical
procedure to restore joint function. Joint replacement surgery involves the
placement of manufactured components that do not last indefinitely. The greater
the functional demands on the prosthesis, the shorter its mechanical life. Older
patients with chronic arthritis pain tend to have lower expectations and place
lower demands on joint replacements than younger posttrauma patients who
have had no previous joint disability and may have higher expectations of return
to function. Approximately 3% of the adult population in the United States is
living with one or more joint replacements. The demand for all joint
replacements has been increasing, a trend that is expected to continue as the
population ages, technology improves, and indications broaden.3
•
FIGURE 21.3 Limb rotation evaluation for a patient with a left femoral shaft fracture
fixed by a locked intramedullary rod. Rotatory misalignment was noted as soon as the
patient attempted to stand. A, For the right femur, the angle between the femoral neck
and horizontal is 18.9°. B, The angle between the femoral condyles and horizontal is
3.8°. The femoral neck is anteverted, and the anteversion angle is 15.1°. C, For the
left femur, the angle between the femoral neck and horizontal is 22.8°. D, The angle
between the femoral condyles and horizontal is 45.6°. The femoral neck is
retroverted, and the retroversion angle is 22.8°.
•
FIGURE 21.4 Rotational osteotomy. A, Following treatment of femoral shaft
fracture, the left femoral neck was found to be retroverted. B and C, After retrieval of
the intramedullary (IM) rod, an intramedullary bone saw was introduced to make a
transverse osteotomy through the femoral shaft. D, The femur was rotated the
appropriate amount to correct the retroversion and fixed with another locked IM rod.
•
FIGURE 21.5 Vascularized fibular autograft and core decompression for treatment
of osteonecrosis. Anteroposterior radiograph shows the femoral head is sclerotic and
a crescent sign is visible. The graft has been secured with a K-wire.
•
FIGURE 21.6 Hip arthrodesis. Anteroposterior radiograph of pelvis shows right hip
arthrodesis (arrow) and left total hip replacement.
Arthroplasty
An arthroplasty is a surgical repair of a joint.1,2 There are different types of
arthroplasties, including resection arthroplasty, resurfacing arthroplasty,
interpositional arthroplasty, and partial and total replacement arthroplasty.
Postoperative radiographs that document the immediate results of surgery should
be kept indefinitely and compared with subsequent follow-up radiographs to
detect bone remodeling, changes in position and alignment of components,
loosening, and other complications. CT, MRI, sonography, and nuclear imaging
are occasionally useful for problem-solving but are generally unnecessary on a
routine basis for postsurgical arthroplasty patients.
•
FIGURE 21.7 Girdlestone procedure, where the femoral head and neck have been
resected.
Resection arthroplasty involves excision of one or both of the articular

surfaces, leaving the ends of the bone to articulate with each other. Because the
joint is not fixed, a pseudoarthrosis develops, preserving motion. At the hip, a
resection arthroplasty is called a Girdlestone procedure (Figure 21.7) and may be
used in circumstances where a prosthesis is unsuitable, such as active infection.
Joint Replacement Materials

Metal, polyethylene, and cement are commonly used in joint replacements.4
Metal components—usually titanium or a cobalt-chromium alloy—are used for
strength and stiffness. The fatigue strength of these metals under cyclic loading
is such that in vivo failure is rare. Ultrahigh-molecular-weight polyethylene is
used for concave articular surfaces such as the acetabulum, tibial plateau, and
glenoid fossa. This material is denser and stiffer than the polyethylene used in
common kitchenware and is manufactured to have high resistance to abrasive
wear. A metal back is often used to provide mechanical support. Polyethylene is
radiolucent—like other plastics—but the presence of a metal back, especially at
the acetabulum, may obscure the polyethylene on radiographs. Many
polyethylene components have embedded metal markers that indicate their
position on radiographs. Bone cement (polymethylmethacrylate or
methylmethacrylate) is a rapidly polymerizing acrylic plastic that is used as an
adhesive to fix metallic or polyethylene components to bone. Cement is rendered
radiopaque during manufacture by the addition of barium sulfate. Ceramics have
become more popular for use as articular surfaces. For the small joints of the
hands and feet, silicone rubber prostheses may be used. Recently, pyrolytic
carbon components have been introduced for use in the hand.
Implanted metal components are often fixed into bone with cement. Bubbles
in the cement that might act as stress risers are removed before use by
centrifugation or vacuum chamber, and the cement is injected into the medullary
space under high pressure. A polyethylene plug at the bottom of the prepared
cavity creates a closed space and prevents flow of cement down the medullary
canal. Metal prostheses that are implanted without cement may have a
mechanical press fit that provides immediate stability and a specially textured
surface (porous coat) that allows ingrowth of bone or fibrous tissue, providing
eventual long-term fixation. A high degree of precision is ensured at surgery
through the use of jigs, cutting guides, and mock-ups that allow the surgeon to
achieve a perfect geometric fit between the bone and prosthetic component.
Screws temporarily secure some cementless components until bone ingrowth
occurs. Hydroxyapatite crystals applied to the surfaces of cementless metal
components during manufacturing may improve biologic fixation in bone. The
crystalline coating of the prosthesis is directly incorporated into the molecular
structure of the host bone.
•
FIGURE 21.8 Resurfacing hemiarthroplasty of the hip.
Because different materials deform to different degrees under mechanical

loading (their stiffness is different), shear stresses develop at the interfaces,
particularly between bone and metal or bone and cement. A layer of fibrous
tissue that grows into these interfaces helps dissipate the forces by redistributing
them over a greater surface area. This layer is similar to the periodontal ligament
that cushions the teeth in the softer cancellous bone of the jaws. The fibrous
layer may be visible on radiographs as a fine lucency (no more than 2 mm thick)
between bone and cement or bone and metal. An additional area of increased
stress is the interface between cement and metal; microscopic motion may occur
at this interface, but no gap should be seen.
Hip Replacement
There are several general types of hip replacements.5,6 A resurfacing arthroplasty
resurfaces the articular surface of the femoral head with a metal cup (Figure
21.8). Hemiarthroplasties of the hip replace the femoral head and neck (Figure
21.9). Unipolar femoral prostheses compose a single metal component with a
stem that is fitted into the medullary canal and a head that articulates with the
native acetabulum. Bipolar femoral prostheses have a metal femoral component
comprising a stem and a head and an acetabular component comprising a metal
socket with a polyethylene liner. The metal socket articulates with the native
acetabulum, and the head of the femoral component articulates with the
polyethylene liner. Although the acetabular component is not fixed, most of the
motion takes place between the head and liner, preserving the native acetabular
cartilage. Hemiarthroplasties are used for disease of the proximal femur in which
the acetabulum is relatively normal. For example, a femoral neck fracture
complicated by osteonecrosis might be managed with a bipolar femoral
prosthesis. A bipolar prosthesis may be converted to a total hip replacement
(THR) with interchangeable components. A THR has both femoral and
acetabular components that replace the native articular surfaces (Figures 21.10
and 21.11). Most currently implanted prostheses have a metal acetabular
component with a polyethylene liner that forms the articular surface. The
components may be fixed to the bone with or without cement. Some surgical
approaches require an osteotomy of the greater trochanter for exposure; it is
usually reattached with wires or cables. If a nonunion develops, a lurching gait
results. If a gluteal soft-tissue release is used for surgical exposure, the gluteal
musculature may be reattached to the greater trochanter with sutures, screws
with washers, or soft-tissue anchors. Bone graft and specialized hardware may
be inserted to buttress a deficient proximal femur or acetabulum.
•
FIGURE 21.9 Bilateral femoral endoprostheses, unipolar on the right, and bipolar
on the left.
The most common early complication of THR is dislocation (Table 21.1).6,7

Typically, the femoral head rotates externally out of the acetabulum (Figure
21.12). Loss of fixation of the acetabular cup may allow it to dislocate from the
acetabular bed (Figure 21.13). Heterotopic bone formation after THR is
common; it may occasionally interfere with motion (Figure 21.14). Osteolysis in
total joint replacements is usually caused by foreign body granulomatous
reaction. The mechanical friction of the metal on polyethylene abrades
microscopic particles of polyethylene, which incite an osteolytic granulomatous
foreign body reaction. Migration of polyethylene debris and its accompanying
reaction along cement-bone or metal-bone interfaces—often in the form of a thin
membrane—may eventually cause gross loosening. Massive localized osteolysis
may also occur; these lesions are filled with the same polyethylene foreign body
reaction that causes component loosening. Polyethylene osteolysis usually
progresses slowly over many years. Debris may pass through lymphatics to
regional lymph nodes. Because the radiolucent polyethylene liners of total joint
replacements are responsible for the joint space on radiographs, thinning or gross
failure of the polyethylene is evident on radiographs as narrowing of the joint
space (Figure 21.15). Radiographic findings that suggest loosening of prosthetic
components include widening of the lucent zone at the cement-bone or metal-
bone interfaces to greater than 2 mm, migration of components from their
original positions, development of a lucent gap between metal and cement,
cement fracture, periosteal reactive bone, and osteolysis. Any gap between metal
and cement is abnormal (Figure 21.16). A gap of more than 2 mm between bone
and metal or bone and cement is abnormal. However, a component may not be
clinically loose or symptomatic until the gap surrounds the component
completely. With radiography, only the interface that is in tangent to the X-ray
beam can be confidently assessed. Fragmentation of cement seems to be the
result of mechanical failure rather than a biologic process.
•
FIGURE 21.10 Total hip replacements (THRs) (different patients). A, Noncemented
right THR. B, Cemented left THR.
•
FIGURE 21.11 Total hip replacements (THRs) (different patients). A, Noncemented
THR with metal-on-metal bearing surface. B, Noncemented THR with ceramic head
(arrow).
Table 21.1 COMPLICATIONS OF JOINT REPLACEMENT
Fracture
Dislocation
Polyethylene wear or failure
Osteolysis
Metallosis
Infection
Loosening
Stress fracture
Neurovascular injuries
Thromboembolism
Some prostheses have eliminated the polyethylene acetabular liner from their
designs, replacing it with metal or ceramic liners. These prostheses therefore
have ceramic-on-ceramic or metal-on-metal bearing surfaces. A particular
disadvantage of the metal-on-metal bearing in hip replacement is the release of
large amounts of very small wear particles and metal ions. The deposition of
metallic wear particles in periprosthetic tissues induces a spectrum of changes.
Periprosthetic soft-tissue lesions have been described variously as aseptic
lymphocytic vasculitis–associated lesions, adverse reaction to metal debris, and
pseudotumors. Radiographs usually show normal findings, but in advanced cases
there may be evidence of loosening or femoral neck narrowing in resurfacing
arthroplasty. Cystic or solid masses can be detected on MRI, CT, and
ultrasonography (Figure 21.17). Complications not directly related to the
prosthesis itself may occur, such as stress fractures following the resumption of
physical activity made possible by the hip replacement (Figure 21.18).
•
FIGURE 21.12 Dislocated total hip replacement. The head has moved laterally and
superiorly.
•
FIGURE 21.13 Dislocation of the acetabular cup from the acetabular bed, with
dislocation of the femoral head from the cup.
•
FIGURE 21.14 Heterotopic ossification in bilateral total hip replacements.
•
FIGURE 21.15 Total hip replacement with osteolysis (white arrow) around the
acetabular cup and proximal lateral femoral stem. The head is asymmetrically
positioned (black arrow) within acetabular cup indicating polyethylene failure.
•
FIGURE 21.16 Loose cemented total hip replacement with failure of the cement-
metal bond of the femoral component (arrows).
•
FIGURE 21.17 Total hip replacement (THR) with aseptic lymphocytic vasculitis–
associated lesions. Coronal T1 MRI shows an ovoid soft-tissue lesion adjacent to the
greater trochanter (arrow) in a patient with a metal-on-metal THR.
•
FIGURE 21.18 Anterior view of radionuclide bone scan of a patient with bilateral
total hip replacements. A stress fracture was present in the lateral femoral cortex on
the left (arrow).
•
FIGURE 21.19 Measurement of tibial tubercle-trochlear groove (TT-TG) distance on
MRI. A, Superimposed axial images of the tibia and femur showing TT-TG distance. B
and C, Alternative method of determining TT-TG distance by measuring from the
edge of image (or other common landmark) and subtracting. Simple geometry may be
used to correct for rotation of the limb but is unnecessary in our experience.
KNEE SURGERY
Extensor Realignment
Anterior knee pain may be related to patellar instability in which the extensor
mechanism tends to displace the patella laterally during extension because the
infrapatellar tendon is misaligned with the trochlea. One manifestation of this
misalignment is the distance between the tibial tubercle and the trochlear groove
in the condylar line of the femur; this distance is normally much less than
20 mm, and it may be measured on axial CT or MRI (Figure 21.19). Surgical
realignment of the mechanical axis of the quadriceps mechanism involves
changing the location of the anterior tibial tubercle, which receives the
infrapatellar tendon insertion. In most cases, the tibial tubercle is relocated
medially to address lateral patellar subluxation (Figure 21.20).
Osteotomy
A high tibial valgus osteotomy is a common treatment for severe medial
compartment osteoarthritis with varus deformity (Figure 21.21).1,2 By realigning
the tibial shaft, the varus deformity is corrected, and the mechanical axis of the
knee is restored. This has the effect of reducing the weight-bearing stress on the
diseased medial compartment and redistributing some of it to the lateral
compartment. Distal femoral varus osteotomies can correct valgus deformities at
the knee from lateral compartment osteoarthritis.
Knee Replacement
The most common total knee replacement (TKR) has a bicondylar femoral
component, a tibial component, and a patellar component (Figure 21.22).8,9 The
tibial and patellar components have polyethylene articular surfaces. Some
designs incorporate meniscal bearings that move with flexion and extension,
attempting to duplicate more closely the normal kinematics of the knee (Figure
21.23). Unconstrained TKRs depend on the muscles and ligaments of the knee
for stability. A semiconstrained or intercondylar-stabilized TKR has a post that
extends vertically from the tibial component into a slot in the bicondylar
component (Figure 21.24). This mechanism partially constrains the allowable
motion of the prosthesis. If the soft-tissue supports of the knee are poor or have
been sacrificed, a fully constrained (rotating hinge) prosthesis may be used
(Figure 21.25). Because the normal knee rotates as it flexes, rotating hinge TKRs
have a second articulation comprising a metal post that inserts into a
polyethylene socket that allows rotation. The bone stock of the tibia is
sometimes deficient because of previous high tibial osteotomy; bone graft may
be used to supplement it. Cement is typically used as a surface adhesive to fix
the components to the bone. The ideal alignment of the tibial articular surface is
parallel to the floor; this is best demonstrated on standing radiographs.
•
FIGURE 21.20 Anterior tibial tubercle realignment surgery. The mechanical axis of
the quadriceps mechanism has been changed by moving the insertion of the
infrapatellar tendon medially. A, Lateral radiograph. B, Anteroposterior radiograph.
•
FIGURE 21.21 High tibial valgus osteotomy with internal fixation. An opening
wedge was performed, internally fixed, and filled with bone graft.
A unicondylar TKR is used when there is significant, symptomatic disease of

either the medial or lateral compartment but relative preservation of the other
compartments. Both sides of the joint of the involved compartment are replaced
(Figure 21.26). The components are typically cemented in place. The bearing
surface is polyethylene. The stability of these prostheses depends on the inherent
stability of the host knee; the surgery can be accomplished with the preservation
of both the anterior cruciate ligament and posterior cruciate ligament. The cost is
lower than that of a bicondylar TKR, and the rehabilitation is typically easier.
The long-term results are less predictable, because intervening disease of the
remaining compartments often leads to revision to a bicondylar TKR.
Most complications of knee replacements involve the patellar component
(Figure 21.27).10,11 Major trauma to limbs with prosthetic joints may result in
fractures and dislocations. When fractures occur, they usually begin at a bone-
metal interface that acts as a stress riser (Figure 21.28). Polyethylene wear and
gross fragmentation of the polyethylene bearing surface of the tibia may occur
(Figure 21.29). Polyethylene wear can be recognized on radiographs as loss of
joint space on weight-bearing views. Some polyethylene inserts have metal
wires embedded within them, and displacement of these wires signifies
displacement of the polyethylene. Polyethylene loss from the patellar component
is difficult to recognize without axial (sunrise) patellar radiographs. Metal
particles are also found around joint implants and may be carried to regional
lymph nodes. Synovial discoloration is common around prostheses (seen at
revision arthroplasty, not on imaging), and the deposition of metal particles has
been associated with synovitis (Figure 21.30). Other biologic effects of
metallosis are suspected but not proved. Osteolysis may occur around TKRs,
similar to the situation at the hip (Figure 21.31). Infection is an uncommon
complication that often requires arthrocentesis for diagnosis. Soft-tissue swelling
with a new effusion is a typical but nonspecific radiographic sign of infection. If
organisms are not cultured from the joint fluid at arthrocentesis, an open
synovial biopsy may be necessary. Infection of a prosthesis typically leads to its
removal.
•
FIGURE 21.22 Bicondylar total knee replacement. A, Lateral radiograph. B,
Anteroposterior radiograph.
•
FIGURE 21.23 Bicondylar total knee replacement with meniscal bearings. A,
Lateral radiograph. B, Anteroposterior radiograph. Meniscal bearings have metal
markers (arrows in B).
FIGURE 21.24 • Intercondylar-stabilized total knee replacement. A, Lateral

radiograph. B, Anteroposterior radiograph. A radiolucent post extends vertically from
the tibial component into a slot in the bicondylar component (arrow in B).
•
FIGURE 21.25 Rotating hinge total knee replacement. A, Lateral radiograph. B,
ANKLE SURGERY
Ankle Arthrodesis
Arthroplasties of the ankle are usually reserved for patients with severe pain
from degenerative arthritis, most commonly posttraumatic. Other possible
indications include osteonecrosis of the talar dome, primary osteoarthritis,
chronic instability, and inflammatory or postinfectious arthropathy. Ankle
arthrodesis is fusion of the tibiotalar joint. When performed as primary
treatment, the articular surfaces are removed to promote healing and the tibia is
fixed to the talus. The distal fibula is mobilized for surgical exposure and then
applied to the fusion site. If indicated, subtalar arthrodesis may be performed at
the same time (Figure 21.32). If ankle arthrodesis is performed to salvage a
failed prosthesis or an osteonecrotic talus, allograft bone is generally used to fill
the resulting space left by retrieval of the prosthesis or debridement of the
necrotic bone. One radiologically striking option is the use of a femoral head
allograft (Figure 21.33).
FIGURE 21.26 • Unicompartmental total knee replacement with cemented
polyethylene tibial component. A, Lateral radiograph. B, Anteroposterior radiograph.
•
FIGURE 21.27 Total knee replacement with loosening of patellar component. A,
Postoperative radiograph. B, Follow-up radiograph several months later shows
resorption of bone at cement-bone interface of patellar component (arrow).
Ankle Replacement
Ankle replacement arthroplasty is becoming more prevalent with several devices
receiving approval from the Federal Drug Administration in the past few years
and becoming available for general use. Component designs of total ankle
replacement systems can be classified by several factors such as bearing type
(fixed vs mobile bearing), bearing material (polyethylene vs ceramic), resurfaced
articulation (superior, medial, lateral), and constraint (constrained,
semiconstrained, and nonconstrained).12 Early generations of ankle prostheses
were unsuccessful and had high failure rates. Contemporary third-generation
designs consist of 3 components: a metallic tibial base plate, a metallic talar
component, and an ultrahigh-molecular-weight polyethylene bearing (Figures
21.34–21.37). These prostheses replace the tibial plafond and the talar dome but
require an intact native ankle mortise. Ankle replacements are subject to the
same complications as found in other joints, but radiologists should be
particularly alert to subsidence of the talar component.13,14 Subsidence of the
talar component occurs when the metal sinks below the surface of the talar
osteotomy (Figure 21.38), seen on lateral radiographs. Comparison with
immediate postoperative radiographs is always helpful.
•
FIGURE 21.28 Fracture of femur through stress riser at the superior edge of the
femoral component.
•
FIGURE 21.29 Total knee replacement with polyethylene thinning in the medial
compartment (arrow).
•
FIGURE 21.30 Total knee replacement with metal synovitis. A, Lateral radiograph
shows increased radiodensity in the suprapatellar recess (arrow) from deposition of
metal in the synovium. B, Axial CT shows metallic deposition within the synovium of
the suprapatellar recess.
TUMOR RECONSTRUCTION
Bone lesions may be resected piecemeal or en bloc. Incisional procedures
involve cutting through the lesion itself and, typically, removing it in pieces.
Curettage is a procedure of scooping out the contents of a lesion using a
spoonlike instrument called a curet.1,2 Sometimes, physical or chemical
treatments, such as cryotherapy, are applied to the surgical bed in an effort to
eradicate residual lesional tissue. Reconstruction after curettage is typically
packing with autograft or allograft bone chips (Figure 21.39) or
methylmethacrylate cement (Figure 21.40). An alternative to packing bone
defects with bone chips or methylmethacrylate cement is the use of calcium
sulfate bone graft substitute, a resorbable material that acts as a scaffold for the
formation of new bone. As the new bone forms, the calcium sulfate is resorbed
by the body. Over a period of 2 or 3 months, the radiopaque material disappears
and is replaced by a faint rim of new bone formation that continues to grow and
remodel after the bone graft substitute is gone (Figure 21.41). The calcium
sulfate pellets may also be impregnated with antibiotics for use in an infected
bone defect.
•
FIGURE 21.31 Total knee replacement with osteolysis. Anteroposterior radiograph
shows extensive periprosthetic osteolysis around the metal-cement interface of the
tibial plate with loosening.
•
FIGURE 21.32 Ankle and subtalar arthrodesis with locked intramedullary rod
fixation.
•
FIGURE 21.33 Ankle and subtalar arthrodesis with femoral head allograft (different
patients). A, Sagittal CT shows arthrodesis with femoral head allograft and locked
intramedullary (IM) rod. B, Anteroposterior radiograph shows femoral head allograft
(arrow) and locked IM rod. An electric stimulator is in place.
Excisional resections typically remove the lesion en bloc. A marginal excision

cuts around the gross margin of the lesion and may leave microscopic residual. A
wide excision removes a cuff of normal tissue in continuity with the lesion and is
intended to provide tumor-free margins. Segmental resections remove part of a
limb but leave the distal portion. Amputations sacrifice the distal portion of an
entire extremity and are named for the level at which the limb is transected. For
example, a below-knee amputation is an amputation of the leg at the level of the
proximal tibia. It is possible for an amputation to be incisional or excisional
depending on the level of the amputation relative to the tumor site. Saucerization
is a procedure in which the medullary cavity is exposed widely, typically for
drainage of a bone abscess.
•
FIGURE 21.34 Total ankle replacement with Salto-Talaris prosthesis. A, Lateral
radiograph. B, Anteroposterior radiograph.
•
FIGURE 21.35 Total ankle replacement with INBONE II prosthesis. A, Lateral
Reconstruction after tumor resection may be challenging because of the large

size of the resulting defect. Massive allografts can be transplanted as intercalary
segments or blocks or as entire intact structures, including an articular surface
(Figure 21.42) or joint. Mechanical complications and failures are common with
osteoarticular allografts15; therefore, intercalary allografts preserving the native
joint are preferred when possible.16 When large allografts are used, the biologic
effect is similar to an organ transplant rather than a tissue transplant. Direct
remodeling of large allografts that begins at the graft-host junction may
ultimately encompass the entire implant after months or years. Graft failure is
recognized when there is progressive resorption of the graft or failure to unite to
the host bone. The alternative to a massive allograft is often a modular total joint
replacement, in which resected bone and joints are replaced with prostheses
(Figure 21.43).17 For reconstruction involving the knee, because the support
soft-tissue structures may be sacrificed in the tumor resection, rotating hinge
prostheses are favored (Figure 21.44).
FIGURE 21.36 • Total ankle replacement with Infinity prosthesis. A, Lateral

FIGURE 21.37 • Total ankle replacement with STAR prosthesis. The STAR
prosthesis has a polyethylene bearing with two wire markers that moves
independently between the metal tibial and talar components. A, Lateral radiograph.
B, Anteroposterior radiograph.
FIGURE 21.38 • Total ankle replacement with aseptic loosening. The tibial
component is loose with gaps between bone and metal. There is extensive sclerosis
of the distal tibial from the mechanical stress resulting from the loosening. There is
subsidence of the talar component, where the metal has sunk below the surface of
the talar osteotomy. A, Lateral radiograph. B, Anteroposterior radiograph.
•
FIGURE 21.39 Bone chips packing site of curettage for enchondroma.
•
FIGURE 21.40 Methylmethacrylate cement in curettage site for giant cell tumor of
bone.
•
FIGURE 21.41 Bone graft substitute with progressive incorporation. A, Immediate
postoperative radiograph. B, Radiograph 2 months after surgery.
•
FIGURE 21.42 Anteroposterior (A) and lateral (B) radiographs of the proximal lower
leg demonstrate massive intercalary tibial allograft for tumor reconstruction after
segmental tibial shaft resection. Surgical drains are still in place.
•
FIGURE 21.43 Oncologic bipolar hip replacement for tumor reconstruction after
resection of an osteosarcoma from the intertrochanteric region of the proximal femur.
FIGURE 21.44 • Oncologic rotating hinge total knee replacement for tumor
reconstruction after resection of an osteosarcoma involving the distal femur and knee.
A, Lateral radiograph. B, Anteroposterior radiograph.
Following tumor treatment, imaging modalities for surveillance are chosen

based on the type of resection performed, the nature of the complication being
monitored for, and individual patient variables, such as tumor type or certain
imaging contraindications (eg, inability to undergo MRI because of a
pacemaker). Radiographs, CT, and MRI are useful for following bone tumor
resection sites for tumor recurrence. CT and radiographs can also evaluate for
periprosthetic fracture and hardware failure. For soft-tissue tumor resection,
MRI tends to be more useful than CT for tumor recurrence monitoring because
of improved soft-tissue characterization. Doppler ultrasonography can be used to
assess for local soft-tissue tumor recurrence when MRI is not an option, because
recurrent tumor tends to have higher vascularity than the background soft
tissues. There are no widely accepted evidence-based guidelines for the timing
of recurrent and metastatic disease surveillance because of variability in tumor
type, location, and grade.
References
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3. American Academy of Orthopaedic Surgeons website (orthoinfo.aaos.org). Accessed June 27, 2017.
4. Morrey BF, Berry DJ, An K-N, Kitaoka HB, Pagnano MW, eds. Joint Replacement Arthroplasty: Basic
Science, Hip, Knee, and Ankle. 4th ed. Lippincott Williams & Wilkins; 2012.
5. Mulcahy H, Chew FS. Current concepts of hip arthroplasty for radiologists: part 1, features and
radiographic assessment. AJR Am J Roentgenol. 2012;199(3):559–569. doi:10.2214/AJR.12.8843
[PMID:22915395].
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[PMID:22915396].
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2006;29(21):1–6.
12. Mulcahy H, Chew FS. Current concepts in total ankle replacement for radiologists: features and imaging
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[PMID:26496551].
13. Mulcahy H, Chew FS. Concepts in total ankle replacement for radiologists: complications. AJR Am J
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Am J Roentgenol. 2013;200(6):1310–1316. doi:10.2214/AJR.12.9649 [PMID:23701070].
15. Bus MP, van de Sande MA, Taminiau AH, Dijkstra PD. Is there still a role for osteoarticular allograft
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1. Rotational malalignment is suspected in the femur after fixation of a femoral

shaft fracture by locked intramedullary rod. Which imaging modality would be
most appropriate for determining the degree of femoral anteversion in this
circumstance?
A. Anteroposterior and lateral radiography of the affected femur
B. Weight-bearing anteroposterior radiography of lower extremities
C. CT including both hips and knees
D. MRI of the affected hip and knee
2. Which of the following radiographic findings most strongly suggests a failing

hip replacement?
A. Lack of separation at the metal-cement interface
B. Bone remodeling at the medial femoral neck cortex
C. Worsening osteoarthritis in the contralateral hip
D. Asymmetric position of femoral head in acetabular cup
3. Which of the following types of arthroplasty is most likely to be used in the

primary treatment of acute trauma?
A. Total knee
B. Bipolar hip
C. Total ankle
D. Unicondylar knee
4. Osteolysis around a total joint replacement is often a biologic process related

to which material?
A. Polyethylene
B. Titanium
C. Methylmethacrylate
D. Hydroxyapatite

1. C Femoral anteversion may be measured from CT scans of the hip and knee.
2. D Asymmetric position of the femoral head in the acetabular cup suggests
failure of the polyethylene liner.
3. B Bipolar hip hemiarthroplasty may be used to treat femoral neck fractures.
4. A Osteolysis is related to polyethylene particles.
22
Imaging of the Postsurgical Upper
Extremity
Felix S. Chew
This chapter discusses the postsurgical radiology of common operations of the

upper extremity.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of the postsurgical upper extremity,
4. summarize relevant concepts and knowledge for the following topics: shoulder arthroplasty,
elbow arthroplasty, wrist arthroplasty, and hand arthroplasty.
ARTHROPLASTY
An arthroplasty is a surgical procedure to restore joint function. There are
different types of arthroplasties, including resection arthroplasty, resurfacing
arthroplasty, interpositional arthroplasty, and partial and total replacement
arthroplasty. Postoperative radiographs that document the immediate results of
surgery should be kept indefinitely and compared with subsequent follow-up
examinations to detect bone remodeling, changes in position and alignment of
components, loosening, and other complications. CT, MRI, sonography, and
nuclear imaging are occasionally useful for problem-solving but are generally
not needed on a routine basis in arthroplasty patients.
According to the American Academy of Orthopaedic Surgeons Web site
(orthoinfo.aaos.org), approximately 600 000 knee replacements and 300 000 hip
replacements are being performed annually in the United States, compared with
53 000 shoulder replacements and 3000 elbow replacements. Joint replacement
surgery involves the placement of manufactured components that do not last
indefinitely. As with joint replacements in the lower extremities, the greater the
functional demands on the prosthesis, the sooner its mechanical failure. Older
patients with chronic arthritis pain tend to have lower expectations and place
lower demands on joint replacements than younger posttrauma patients who
have had no previous joint disability and may have higher expectations of return
of function.
SHOULDER ARTHROPLASTY
The primary indication for shoulder arthroplasty is painful, disabling arthritis of
the glenohumeral joint.1 Preoperative radiographic evaluation is typically
obtained with the patient in the upright position. The Grashey view
(anteroposterior oblique radiograph that displays the glenohumeral joint in
profile) is particularly useful in both preoperative planning and postoperative
follow-up. Following arthroplasty, the glenohumeral joint will be obscured by
the prosthesis and the anteroposterior radiograph becomes less helpful. CT, MRI,
and sonography are useful in special circumstances, both before and after
arthroplasty. When the rotator cuff function is adequate and symptoms are
caused by glenohumeral arthritis, options for implants include resurfacing
hemiarthroplasty, anatomic hemiarthroplasty, and anatomic total shoulder
arthroplasty. In resurfacing hemiarthroplasty, the articular surface of the humeral
head is replaced by a metal or pyrocarbon component. The implant may replace
the entire articular surface (Figure 22.1) or just a portion (Figure 22.2). The
glenoid articular surface is not replaced and the humeral tuberosities with their
muscle insertions are left intact. In the anatomic hemiarthroplasty,2 the humeral
head is resected across the anatomic neck and the medullary cavity is prepared to
receive a metal humeral head prosthesis (Figure 22.3). The stem may be fixed by
cement or may have a porous coating for subsequent bony ingrowth. The glenoid
surface may be reshaped to fit the humeral head component better. A glenoid
component, usually polyethylene fixed by cement, may be included to comprise
a total shoulder replacement (Figure 22.4). There is typically a metal marker in
the glenoid polyethylene that makes it easier to identify on radiographs. Some
shoulder glenoid components have a metal back and a polyethylene liner. The
stability and function of resurfacing and anatomic shoulder replacements depend
on the surrounding soft-tissue structures because the prostheses are
unconstrained. The rotator cuff remains attached to the greater and lesser
tuberosities.
The reverse total shoulder replacement puts the ball on the glenoid (called the
glenosphere) and the socket on the humerus (called the humerosocket) (Figure
22.5), the opposite of normal anatomy.2,3 Rotator cuff tear arthropathy is the end
result of chronic massive rotator cuff tears, in which rotator cuff dysfunction
results in glenohumeral arthropathy. With loss of rotator cuff function, the
humeral head becomes unstable from the loss of balanced muscle tension that
helps maintain its position within the shallow glenoid socket. Abnormal wear
patterns and secondary degenerative changes develop in the glenohumeral joint.
Superior migration of the humeral head may result in impingement of the greater
tuberosity on the undersurface of the acromion with erosion and remodeling of
the acromion and distal clavicle into an acetabular-like socket
(acetabularization). The reverse shoulder prosthesis provides a fixed fulcrum at
the glenoid that neutralizes this instability and eliminates the abutment of the
humerus on the acromion. This arrangement is also more stable than the
anatomic shoulder replacement when there is inferior, anterior, posterior, or
multidirectional glenohumeral subluxation. By shifting the center of rotation of
the shoulder medially and lengthening the humerus, the reverse shoulder
prosthesis allows the deltoid to elevate and rotate the arm in place of the
deficient rotator cuff. Reverse prostheses may also be used when failed anatomic
prostheses are revised. The various reverse prostheses differ mainly in the size
and shape of the glenosphere and its manner of fixation to the scapula. The
glenoid component is modular with a cementless baseplate fixed by screws and
an attached glenosphere. The humeral components have a polyethylene liner in a
metal socket and an intramedullary stem that is typically cemented. The large
size of the humeral component may lead to scapular notching, in which the metal
edge of the humeral component repetitively impinges on the lateral border of the
scapular body in adduction. This may be recognized on radiographs by a notch
in the medial scapular border just inferior to the glenosphere (Figure 22.6).
Another complication that is unique to reverse shoulder arthroplasty is stress
fracture of the scapular spine, the result of overuse of the deltoid musculature in
place of the rotator cuff. Reverse shoulder replacements are also subject to the
usual arthroplasty complications of dislocation, aseptic loosening, hardware
failure, periprosthetic fracture, and infection.
•
FIGURE 22.1 Shoulder resurfacing hemiarthroplasty in a 55-year-old man. The
prosthesis is made of cobalt-chromium alloy with titanium undersurface coating for
bone ingrowth and has a central stabilizing post. The prosthesis replaces the humeral
articular surface and articulates with the native glenoid.
Oncologic shoulder replacements are used to reconstruct the proximal

humerus after tumor resection. They are typically modular components that
consist of a humeral head, a proximal shaft, and a distal humeral stem. The
components are sized to match the length of the resection (Figure 22.7). Massive
allograft bone may also be used in conjunction with metal components,
depending on availability and necessity. In patients with reconstructions after
tumor surgery, periodic surveillance is obtained not only for potential
complications arising from the reconstruction but also for tumor recurrence.
When tumor recurrence is suspected, cross-sectional or nuclear imaging may be
helpful.
•
FIGURE 22.2 Partial shoulder resurfacing hemiarthroplasty in a 31-year-old man
with glenohumeral arthropathy. The metal prosthesis replaces a portion of humeral
articular surface and has a tapered, threaded, central stabilizing post for cementless
fixation. A, Anteroposterior radiograph. B, Axillary lateral radiograph.
ELBOW ARTHROPLASTY
Radial head replacements are used as primary surgical treatment for displaced
and comminuted radial head fractures and as secondary treatment for
posttraumatic radiocapitellar osteoarthritis.4,5 Radial head fractures are common
and many occur in young adult patients. The most common radial head implants
are made of metal, either titanium or cobalt-chromium alloys. There are 2
generic designs, the unipolar or monoblock prosthesis (Figure 22.8), which has a
head and fixed stem with no internal motion, and the bipolar prosthesis (Figure
22.9), which has a ball-and-socket joint between the head and the stem. The
stems are pressed into the medullary cavity of the proximal radius and are
generally not secured with cement or screws. On radiographs, the head should
always be aligned with the capitellum and the stem should always be within the
medullary cavity of the radius. Complications include bone resorption around
the stem, secondary osteoarthritis at the radiocapitellar or proximal radioulnar
joints, malalignment, disassembly of components, and overstuffing. Overstuffing
occurs when the prosthesis is bigger than the original radial head and does not
properly fit into the space. The usual complications of loosening, infection,
dislocation, and breakage may also occur. If a silicone prosthesis was used,
synovitis would be a potential complication.
The main indication for total elbow replacement has been end-stage
involvement by rheumatoid arthritis, but total elbow replacement may also be
used for degenerative arthritis or reconstruction after trauma.4–6
•
FIGURE 22.3 Anatomic shoulder hemiarthroplasty in a 72-year-old woman with
glenohumeral arthritis. A, The humeral head has been resected and replaced by a
metal component with noncemented stem. There is no glenoid component. B, Three
years later, the component has subsided into the medullary cavity and the distal stem
has migrated laterally. Bone remodeling is present about the component. The glenoid
is eroded.
•
FIGURE 22.4 Anatomic total shoulder replacement in a 68-year-old woman with
degenerative glenohumeral arthropathy. The glenoid component is polyethylene with
1 bearing surface and 3 pegs that are cemented in place. There is a metal marker in
the central peg. The humeral component is noncemented. A, Grashey radiograph. B,
Axillary lateral radiograph.
•
FIGURE 22.5 Reverse total shoulder replacement in a 62-year-old woman with
reverse left total shoulder replacement (Delta III prosthesis). The baseplate is
cementless and secured by screws that spread away from the center post. The
glenosphere is much larger than the glenoid process. The humerosocket is cemented.
A, Grashey radiograph. B, Axillary lateral radiograph.
•
FIGURE 22.6 Reverse total shoulder with scapular notch in a 57-year-old man who
had a reverse total shoulder replacement (Encore prosthesis) for rotator cuff tear
arthropathy. The baseplate is cementless and secured to the scapula by screws in
parallel orientation. The glenosphere is smaller but deeper than the Delta prosthesis.
The humerosocket is cemented. A, Grashey radiograph. The scapular notch is visible
just inferior to the baseplate of the glenosphere. B, Axillary lateral radiograph.
Unlinked total elbow replacements have humeral and ulnar components that
are not mechanically coupled together (Figure 22.10). The humeral component
replaces the trochlea and has a stem that may be cemented or noncemented. The
ulnar component has a polyethylene bearing surface that fits the trochlear
component. Stability of this prosthesis depends on the proper alignment, intact
ligaments, functional musculature, and good underlying bone stock. The radial
head is typically resected. Unlinked replacements generally fail earlier than
linked replacements, and loosening of the humeral stem is a particular issue.
Linked total elbow replacements are semiconstrained sloppy hinge joints that
replace the humeroulnar joint. Because the components are mechanically
coupled together, the prosthesis provides inherent stability. In addition to simple
flexion and extension, these prostheses designed with laxity to allow small
degrees of rotational and varus-valgus motion, hence designated as sloppy. The
radiocapitellar joint is typically sacrificed. The Coonrad-Morrey prosthesis has
been in use for close to 3 decades and is the prototypic linked elbow prosthesis
(Figure 22.11). The distal anterior flange of the humeral component redistributes
some of the stress of the intramedullary stem on the posterior cortex to the
anterior cortex and provides rotational stability for the component. The ring of
the ulnar component is coupled to the distal humeral yoke by a locking pin, and
polyethylene bushings keep the ring centered within the yoke. The ring has a
polyethylene liner that keeps the pin centered. The bearing surfaces are metal-
on-polyethylene, between the outside of the ulnar ring and the bushings and the
inside of the ulnar ring and the locking pin. Laxity between the bushings and the
ulnar ring allows for the sloppy hinge motion. We commonly see the Biomet
Discover prosthesis in our practice (Figure 22.12). This prosthesis has metal
hemispherical condyles inside the humeral yoke that face the ring of the ulnar
component, which is coupled by a locking pin. The ulnar ring is much larger
than that of the Coonrad-Morrey prosthesis and has a polyethylene liner. The
hemispheric shapes of the internal condyles allow for the sloppy hinge motion.
Long-term outcomes for total elbow arthroplasty are similar to elective hip
replacement, generally better than 90% survival at 10 years. In addition to the
usual complications of pain, loosening, infection (Figure 22.13), polyethylene
wear, and fractures, the disassembly of these complex prostheses may occur
(Figure 22.14).
•
FIGURE 22.7 Oncologic (modular) proximal humerus replacement in a 54-year-old
man with proximal humerus reconstruction following resection of parosteal
osteosarcoma. The prosthesis is modular and assembled from separate head, stem,
and extension components, all available in different sizes for custom fit.
Unicompartmental total elbow replacements may be used for treatment of

radiocapitellar disease. The typical situation for this implant is reconstruction
after trauma. The prosthesis consists of a metal capitellar component and a radial
head component (Figure 22.15). The radial head component may be metal with a
tray for a polyethylene insert, in which case the radiocapitellar articulation is
metal-on-polyethylene and the proximal radioulnar joint articulation is metal-on-
cartilage. Alternatively, a polyethylene head may be attached to the metal radial
stem, providing a polyethylene bearing surface all around. The ulnotrochlear
joint is left intact.
WRIST ARTHROPLASTY
Conditions such as degenerative or inflammatory arthritis, scaphoid nonunion,
Kienbock disease, carpal instability, and scapholunate advanced collapse may
ultimately require arthroplasty.7 The 4-corner fusion is an intercarpal fusion of
the capitate, lunate, hamate, and triquetrum, generally with resection of an
abnormal, symptomatic scaphoid (Figure 22.16). The corners of these 4 bones
normally articulate with each other, hence the name. Proximal row resection may
be used for advanced proximal carpal row disease. The scaphoid, lunate, and
triquetrum are resected and the capitate and hamate are left to articulate with the
radius. The radial styloid may be reduced to avoid impingement with the
shortened carpus (Figure 22.17).
•
FIGURE 22.8 Unipolar radial head replacement in a 74-year-old woman who
sustained radial head and olecranon fractures in a fall. The radial head was replaced
with a noncemented unipolar prosthesis, and the olecranon was internally fixed. A,
Anteroposterior radiograph. B, Lateral radiograph. Loosening, 9 months after
implantation. There is lucency and bone remodeling about the intramedullary stem,
and it has migrated off-center. The olecranon fracture has healed.
•
FIGURE 22.9 Bipolar radial head replacement in a 36-year-old man who sustained
a fracture-dislocation of the elbow in a fall. Radial head replacement was performed
as part of the elbow reconstruction. The prosthesis has a ball-and-socket articulation
between the head and the stem. A, Anteroposterior radiograph. B, Lateral radiograph.
•
FIGURE 22.10 Unconstrained total elbow replacement in a 42-year-old woman with
rheumatoid arthritis. The ulnar component has a polyethylene liner. The radial head
has been resected. Both humeral and ulnar components have been cemented into
their respective intramedullary spaces. A, Anteroposterior radiograph. B, Lateral
radiograph.
Total wrist replacement refers to arthroplasty of the radiocarpal joint with a

prosthetic replacement. The simplest prosthesis is a 1-piece silicone prosthesis.
After the carpus and distal radius are resected, the stems of the prosthesis are
inserted into the medullary spaces of the third metacarpal and distal radius. The
typical candidate for silicone wrist prosthesis is a patient with advanced
manifestations of rheumatoid arthritis who has relatively low mechanical
demands. More elaborate prostheses with metal-on-polyethylene bearing
surfaces may also be used (Figure 22.18), but complications tend to occur much
earlier than with more mature procedures such as hip or knee replacement. The
end of the radius and the proximal carpal row are resected, and metal
components are placed into the distal carpal bones and the distal radius. A
polyethylene cap covers the distal component and provides a polyethylene-on-
metal articulation with the distal radius. The stability of the wrist depends on
static and balanced dynamic soft-tissue supports, and these are frequently
deficient in patients with wrist arthropathy.
•
FIGURE 22.11 Linked total elbow arthroplasty with Coonrad-Morrey prosthesis in a
47-year-old woman with rheumatoid arthritis. Both humeral and ulnar components
have been cemented into their respective intramedullary spaces. A, Lateral
•
FIGURE 22.12 Linked total elbow arthroplasty in a 59-year-old woman with failed
radial head prosthesis that was originally used for reconstruction following radial head
fracture. The prosthesis has hemispherical condyles on the inside of the humeral
yoke facing the ring of the ulnar component, secured together by a locking pin. A,
Lateral radiograph. B, Anteroposterior radiograph.
Wrist fusion is the final option for wrist disability, providing both pain relief
and complete stability but at the cost of mobility. A contoured dorsal plate
typically extends from the distal radius to the third metacarpal shaft, and the
radiocarpal, intercarpal, and carpometacarpal (CMC) joints are fused in neutral
alignment (Figure 22.19). The distal radioulnar joint (DRUJ) is not fused with
the radiocarpal joint, allowing the patient to supinate and pronate the hand.
The DRUJ is the distal articulation between the two forearm bones and, in
conjunction with the proximal radioulnar joint at the elbow, allows supination
and pronation of the hand. Primarily a pivot joint, the radius rotates around the
head of the ulna with a range of motion up to 90°. There are palmar and dorsal
radioulnar ligaments that stabilize the ulnar head in the shallow ulnar notch of
the radius, and distally, there is an articular disk between the head of the ulna and
the carpus called the triangular fibrocartilage. A typical mechanism of injury is a
fall on an outstretched hand. Fractures of the radius or ulna commonly
accompany DRUJ injuries, but isolated DRUJ injuries may also occur. Because
the projected position of the ulnar head relative to the ulnar notch depends in
part on positioning of the parts relative to the X-ray beam and detector,
radiographs may fail to detect instability. In addition, depending on the injury,
instability may occur in only pronation or only supination. Therefore, CT with
the wrist in pronation, neutral, and supination may be helpful in evaluating
instability. Direct imaging of the triangular fibrocartilage and the ligaments may
be accomplished with MRI. Injection of gadolinium-based contrast into the
radiocarpal joint or DRUJ may be helpful in identifying triangular fibrocartilage
tears.
•
FIGURE 22.13 Infected total elbow arthroplasty in a 71-year-old woman with
infected total elbow replacement. The arthroplasty was originally performed for
posttraumatic elbow arthrosis. Erosions of bone are present along the entire cement-
bone interface of the humeral component and along the proximal posterior portion of
the ulnar component. There is extensive periosteal reactive bone along the distal
humeral shaft. The soft tissues are markedly swollen. A, Anteroposterior radiograph.
B, Lateral radiograph.
•
FIGURE 22.14 Total elbow replacement disassembly in a 45-year-old woman who
had sudden pain when reaching out. Presumably, there had been progressive
loosening of the components before the catastrophic failure. A, Anteroposterior
DRUJ hemiarthroplasty is accomplished with an ulnar head replacement

(Figure 22.20). This operation maintains the length of the ulna but relies on the
soft tissues for stability of the joint. The distal end of the prosthesis articulates
with both the triangular fibrocartilage and the ulnar notch of the radius. A metal
and polyethylene component is also available for the radial side of the DRUJ to
complete an unconstrained total joint replacement, but more typically a
constrained prosthesis is used. The Scheker DRUJ prosthesis has a radial
component with a socket into which the distal end of the ulnar component is
inserted (Figure 22.21).8 A polyethylene ball is attached to the end of the ulnar
component and provides a metal-on-polyethylene bearing surface. The
prosthesis provides stability in rotation. The Scheker prosthesis is subject to the
usual complications of metal and plastic prosthetic implants, but the most
common sequel is bone resorption and tapering of the bone around the stem of
the ulnar component. Stress (or traumatic) fractures of the radius may occur at
the intersection of the distal-most screw and the distal post of the radial
component.
•
FIGURE 22.15 Radiocapitellar elbow arthroplasty in a 41-year-old man with
disabling radiocapitellar osteoarthritis. There is a noncemented capitellar component
and a noncemented unipolar radial head component with a polyethylene liner,
providing a metal-on-polyethylene bearing surface at the radiocapitellar joint and a
hemiarthroplasty at the proximal radioulnar joint. A, Lateral radiograph. B,
•
FIGURE 22.16 Four-corner fusion in a 36-year-old man with scaphoid fracture that
progressed to nonunion, proximal pole osteonecrosis, carpal instability, and
secondary osteoarthritis. The scaphoid has been resected and the hamate, capitate,
lunate, and triquetrum have been arthrodesed and internally fixed by 2 Acutrak Mini
screws.
•
FIGURE 22.17 Proximal row carpectomy in a 59-year-old woman with severe wrist
pain due to scapholunate advanced collapse. The scaphoid, lunate, and triquetrum
have been resected, and the capitate articulates directly with the distal radius. The
patient has also had first carpometacarpal arthroplasty with trapeziectomy and tendon
interposition.
FIGURE 22.18 • Total radiocarpal arthroplasty in a 46-year-old woman with
rheumatoid arthritis. There is a polyethylene cap over the distal component that
resembles the shape of the carpus. A, Posteroanterior radiograph. B, Lateral
radiograph.
•
FIGURE 22.19 Carpal arthrodesis in a 59-year-old woman with severe wrist pain
resulting from rheumatoid arthritis. A contoured plate has been placed dorsally for
fixation. A, Posteroanterior radiograph. B, Lateral radiograph.
•
FIGURE 22.20 Ulnar head replacement hemiarthroplasty in a 51-year-old man with
posttraumatic arthropathy of his distal ulna. A, Posteroanterior radiograph. B, Lateral
radiograph.
•
FIGURE 22.21 Distal radioulnar joint (DRUJ) replacement arthroplasty with Scheker
prosthesis in a 21-year-old woman who had disabling arthrosis and instability of her
left DRUJ as sequelae of intra-articular fractures of the distal radius and ulna. The
tapering of the distal ulnar cortex is a reflection of bone resorption and remodeling.
The cortex was of uniform thickness and extended to the distal end of the ulnar stem
immediately after surgery. A, Posteroanterior radiograph. B, Lateral radiograph.
HAND ARTHROPLASTY
The first CMC joint is one of the most common anatomic sites for symptomatic
osteoarthritis. The first CMC joint is a saddle-shaped articulation that permits the
multidirectional dexterity of opposable thumbs as well as grip strength. The
triscaphe joint (trapezium-trapezoid-scaphoid articulation) is frequently involved
as well, so surgical treatments generally include first CMC arthroplasty,
trapeziectomy, and soft-tissue reconstruction (Figures 22.22 and 22.23).9 The
space left by the removal of the trapezium may be filled with autograft tendon,
fat, or costal cartilage, or with a metal, silicone, or pyrocarbon prosthesis.
Tunnels or soft-tissue anchors at the proximal first metacarpal reflect various
soft-tissue reconstructions used to maintain the position of the first metacarpal
base relative to the second metacarpal base.
The metacarpophalangeal joints are commonly involved in rheumatoid
arthritis. End-stage arthropathy may be treated with synovectomy, resection
arthroplasty, and a silicone elastomer prosthesis. The silicone prosthesis is
essentially a 1-piece spacer with tapered plugs on opposite ends that are fitted
into the medullary spaces of the proximal phalanx and metacarpal (Figure
22.24). The implant is not fixed to the bone. Motion across the joint is possible
because the material is flexible and one or both plugs might move in and out of
the medullary spaces like an engine piston. Improvements to the original
Swanson prosthesis include titanium grommets to protect the implant from sharp
bone edges and the incorporation of a more flexible hinge (Figure 22.25).
Silicone particles from mechanical wear may lead to local synovitis and
osteolysis, sometimes requiring implant removal. An anatomic total joint
prosthesis fabricated from pyrocarbon is also available but is much less
frequently seen in our practice.10 The same types of silicone prostheses in
smaller sizes may be used at the proximal interphalangeal and distal
interphalangeal joints, most commonly for posttraumatic degenerative arthritis
(Figure 22.26). Distal interphalangeal joints are more typically fused rather than
replaced. Pyrocarbon prostheses are also available for the interphalangeal joints
(Figure 22.27).
•
FIGURE 22.22 Carpometacarpal arthroplasty in a 66-year-old woman who had
osteoarthritis. The trapezium has been resected. Flexor carpi radialis tendon autograft
has been interposed between the first metacarpal base and the scaphoid and secured
to the first metacarpal by a soft-tissue anchor. A, Posteroanterior radiograph. B,
Oblique radiograph. C, Lateral radiograph.
•
FIGURE 22.23 Carpometacarpal (CMC) arthroplasty in a 54-year-old woman. A,
Posteroanterior radiograph of the wrist shows severe osteoarthritis at the first CMC
joint. B, Intraoperative radiograph shows trapeziectomy with the resulting space filled
by flexor carpi radialis autograft. The 2 metal buttons indicate ligament reconstruction
with composite nonmetallic braided cable spanning the proximal first and second
metacarpals through connecting tunnels. C, Follow-up radiograph shows that the
second metacarpal button has been pulled into the tunnel, indicating loss of fixation.
•
FIGURE 22.24 Silicone metacarpophalangeal (MCP) arthroplasty in a 60-year-old
woman with rheumatoid arthritis who has undergone MCP arthroplasty of the index,
middle, ring, and small MCP joints. There is diffuse osteopenia. Posteroanterior
radiograph of the hand.
•
FIGURE 22.25 Silicone metacarpophalangeal arthroplasty with titanium grommets
in a 45-year-old woman with rheumatoid arthritis. Posteroanterior radiograph of the
hand.
•
FIGURE 22.26 Silicone proximal interphalangeal (PIP) arthroplasty in a 34-year-old
man for posttraumatic osteoarthritis. A, Lateral radiograph. B, Oblique radiograph. C,
Posteroanterior radiograph.
•
FIGURE 22.27 Pyrolytic carbon proximal interphalangeal (PIP) arthroplasty in a 47-
year-old man with pyrolytic carbon replacement at the PIP joint of the middle finger.
The underlying bone and joint deformity was the result of multiple enchondromatosis.
A, Posteroanterior radiograph. B, Oblique radiograph. C, Lateral radiograph.
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1. In patients above the age of 50 years, which radiographic finding is most

closely associated with the use of a reverse prosthesis for shoulder
arthroplasty?
A. Anterior shoulder dislocation
B. Superior humeral head migration
C. Large inferior humeral osteophyte
D. Hypertrophic acromioclavicular osteoarthritis
2. The radiocapitellar joint is typically sacrificed in which type of arthroplasty?

A. Linked total elbow
B. Bipolar radial head
C. Total distal radioulnar
D. Resurfacing
3. Which one of the following types of arthroplasty is most likely to be used in

the primary treatment of acute trauma?
A. Linked total elbow
B. Total radiocarpal
C. Pyrocarbon metacarpophalangeal
D. Unipolar radial head
4. Which type of prosthesis is the least constrained in its motion?

A. Anatomic total shoulder
B. Reverse total shoulder
C. Linked total elbow
D. Scheker total DRUJ
1. B Reverse total shoulder arthroplasty is used when there is rotator cuff
arthropathy, one sign of which is superior humeral head migration.
2. A The radiocapitellar joint is sacrificed in linked total elbow arthroplasty.
3. D Radial head prosthesis are used to treat displaced or comminuted radial
head fractures.
4. A The anatomic total shoulder prosthesis is unconstrained, but the remaining
types are partially constrained.
23
Imaging of Bone Dysplasias in
Adults
This chapter is aimed at the large fraction of you who are neither pediatric
radiologists nor overly fond of dysplasia. It was written to help a general
radiologist quickly interpret the dysplastic bones seen in adults.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of bone dysplasias in adults, the
4. summarize relevant concepts and knowledge for the following topics: radiologic approach to
unknown bone dysplasias, achondroplasia, pseudoachondroplasia, dactyly, enchondromatosis,
Marfan syndrome, multiple hereditary exostoses, neurofibromatosis (NF), osteogenesis
imperfecta, osteopetrosis, osteopoikilosis, osteopathia striata, melorheostosis, and Madelung
deformity.
PART 1: AN APPROACH TO DIAGNOSIS OF BONE
DYSPLASIA IN ADULTS
Why learn about dysplasia? I estimate that only about half of the dysplastic
bones I see in my practice are due to congenital dysplasia. The remaining bones
became dysplastic as a result of some familiar disorders such as trauma, arthritis,
infection, or even surgery. Bone dysplasias are not uncommon. My own gut
feeling for the meaning of “common” comes from growing up in a small, one-
doctor West Texas town of 3000. NF (prevalence ~ 1:3000) is a good example of
a congenital dysplasia that would be likely in our town. Ever since then, I have
continued to use the “common in my village” standard. I now live in the Seattle-
Tacoma-Bellevue metropolitan village of 3.4 million, and “common” for me
now continues to mean something I am likely to see here during the year.
Dysplasias are clinically important. Some dysplasias are associated with an
increased risk of malignancy (multiple hereditary exostoses) or sudden and
premature death (Marfan syndrome). Genetic counseling can be valuable for
family planning. With autosomal dominant dysplasias, such as NF or
achondroplasia, the Mendelian probabilities of having an affected child can be
fairly stark. Radiologists are often viewed as de facto dysplasia experts. I tease
my residents that no matter which subspecialty they pursue, they will end up as a
dysplasia doc. Even if a patient’s diagnosis is well known, they will likely
undergo many follow-up studies during the rest of their lives. Radiographs
represent one of the easiest follow-up studies for a referring physician to order.
As the most prominent organ on most radiographs is the skeleton, one should
expect to look at a lot of bone dysplasia images in one’s career.
I first became aware of the importance of skeletal dysplasias during my
second year of medical school in Houston. My first pediatrics rotation was on
the dysplasia service of Texas Children’s Hospital, which performed most of the
dysplasia consultations in our medical center. Many of the disorders I saw that
month were so rare that I had never heard of them, and I have never seen them
since. My initial reaction was that I was wasting a month that could be better
spent seeing garden-variety pediatric complaints. However, 1 particular child
made the whole month-long rotation worthwhile to me. This little one had been
born with multiple physical anomalies in another country. His parents took him
to a series of very smart and well-trained doctors, who were unanimous that he
would be massively mentally retarded. The parents were heartbroken and
decided to seek a final opinion at our medical center. There were so many
physical findings that the examination and write-up took me several hours. I
presented the case and my differential diagnosis to our team, which was
followed by comments by the intern, the resident, and the dysplasia fellow. Our
attending then carefully explained why all of us and all of the prior physicians
were wrong. “In fact,” he said, “this child can only have the Hallermann-Streiff
syndrome!” We were not terribly impressed by this until he pointed out that,
despite the many physical abnormalities of the Hallermann-Streiff syndrome,
mental retardation was present in only a minority of cases. This much more
hopeful prognosis gave the parents great joy, and my respect for the power of
additional opinions went way up. This experience did not make me want to go
sign up for a dysplasia fellowship. However, it did teach me that making the
right diagnosis can be of great value, even though it leads to no change in the
patient’s treatment. Sometimes giving a good prognosis is a great gift to a
patient. Knowing the correct diagnosis can also be helpful for any future family
planning.
A Quick and Dirty Approach to Skeletal Dysplasias

Since I became a radiologist, I have seen thousands of dysplasia images. This
experience has given me a pretty good idea of which syndromes are common in
most radiology practices. I have used this experience to craft my own 5-step
approach to dysplasia.
Step 1: Could This Be a Dysplasia?

This first step may be the hardest one. There are a lot of physicians out there in
deep denial about dysplasias. They so dislike the idea of having to dictate a
report on a dysplasia case that they may refuse to even put dysplasia on their
mental lists. As soon as they consider the “D” word, up come the visions of bird-
headed dwarves and the hand-foot-uterus syndrome. I have seen some
radiologists actually go through all 5 Kubler-Ross stages of grief1 before settling
down and dealing with a dysplasia case. The goal of this chapter is to help you
learn to stop procrastinating. Avoid denial, anger, bargaining and depression, and
learn to go directly to acceptance.
My advice: Get over it—bird-headed dwarves and hand-foot-uterus syndrome
are pretty darned rare (I am still waiting to see my first case of either one). Better
yet, many cases of dysplasia are actually due to some acquired disorder that you
already know a lot about.
It is helpful to recall the meaning of the word “dysplasia,” which comes from
the Greek roots “dys-” (bad) and “-plasis” (formation). Therefore, if your patient
has bones that are oddly shaped in some way, they are probably dysplastic. As
you look at the shape of a bone and you find yourself subvocalizing words such
as “strange,” “bizarre,” “peculiar,” “odd,” and “weird,” I urge you to train your
brain to automatically translate this into “dysplasia,” “dysplasia,” “dysplasia”...
Once you have come to terms with your patient having a dysplasia, your next
job will be to describe the findings. I find terms such as “genu vara,” “coxa
valga,” “gracile,” “undertubulated,” and “Erlenmeyer-flasking” handy for
describing my findings. Plain English words such as “too big” or “too small”
will work in a pinch. For hard-to-characterize findings, one can always fall back
on the vague but ever-popular “the _______ is somewhat dysplastic…”
Step 2: Could This Be an Acquired Condition?

Do not forget that there are many acquired conditions that lead to dysplastic
bones. This simple concept makes my life a lot easier when I am asked to
consult on an unusual bone case. In my patient population (mostly adults),
acquired disorders are much more common than congenital dysplasia, even
though I work in a large tertiary medical center. Even unusual manifestations of
common, acquired disorders are more common than congenital dysplasias in my
practice. Unless you end up practicing in a large dysplasia referral center, your
experience will probably be a lot like mine.
For growing bones to end up with a normal shape and size, they need normal
muscle pull and gravitational loading. Any process that interferes with this
normal loading may therefore lead to odd-looking bones. Paraplegia or
quadriplegia can provide extreme examples of this. Childhood paraplegics may
end up with extremely gracile (long and thin) bones, with coxa valga, a small
and odd-looking pelvis, and very little muscle mass. Moreover, any chronic
disease that keeps children bedridden during a lot of their growth phase
(leukemia, juvenile chronic arthritis, hemophilia, etc) may leave them with
mildly or significantly dysplastic bones that can be dead ringers for one of the
neuromuscular diseases, such as paraplegia, cerebral palsy, or poliomyelitis.2
Fractures that heal poorly or that have had extensive surgery can appear quite
bizarre at times and should be on one’s mental list of acquired bone dysplasias.
The right bit of clinical history can help one refine one’s differential diagnosis
considerably (Figures 23.1–23.3).
Step 3: Is This a Common Dysplasia?

Unless you are a pediatric radiologist, almost every patient you see with a
congenital dysplasia will have been diagnosed long, long ago by someone wiser
in the ways of dysplasia. If you are fortunate, the referring physician will include
this information on the imaging requisition, eg, “Patient with known tricho-
rhino-phalangeal syndrome—please evaluate for progression.” Otherwise a
quick dumpster-dive through the patient’s electronic medical record will turn up
this information. Alas, some patients arrive from developing nations (such as
West Texas, where I am from) with no medical records and no prior diagnosis. In
these cases, it may be up to you to make the initial diagnosis.
•
FIGURE 23.1 The dysplastic appearance of this bowed and enlarged tibia is due to
Paget disease.
•
FIGURE 23.2 The marked size discrepancy between the left and right ribs and ilium
are due to radiation therapy to the left side during childhood.
•
FIGURE 23.3 The gracile bones and the peculiar soft tissues of the calf here are
due to severe burns this patient received as a child. A, Anteroposterior radiograph. B,
Lateral radiograph.
Taybi and Lachman’s excellent book lists more than 1900 different
syndromes and skeletal dysplasias.3 The mighty Online Mendelian Inheritance in
Man (OMIM) site currently lists 23 916 total entries.4 Sifting through
differential lists of this size are heady wine for the connoisseur of such things.
However, the rest of us prefer a short list of the disorders we are most likely to
see. Years ago, I found guidance from compilations by Kozlowski and
Beighton.5 These authors ranked dysplasias from 0 to 4 stars, corresponding to
their prevalence (4 stars meaning more than 1000 cases in the literature; 3 stars
meaning 100-1000 cases; etc). However, their list was way too long for me, so I
composed my own list of entities I had actually seen within the past year:
Achondroplasia, Dactyly, Enchondromatosis (Ollier), Marfan, Multiple
hereditary exostoses, Neurofibromatosis, Osteogenesis imperfecta, and
Osteopetrosis. I dropped the first letters of each entity into an online anagram
generator,6 and it burped out more than 300 possible mnemonics. Among the
more intriguing were “MADMEN GOOF” and “MEN OF DOGMA.” However,
my current favorite is “OMFG—A DEMON!” Whichever memory device you
use to access this list of possibilities, the next step is to see which one of these
entities is the best fit for your patient. To do this, you actually have to know a
few salient details about each of these entities. These details are presented at the
end of the chapter.
Step 4: Can I Find the Answer in a Text or Online?

Chances are extremely good that the syndrome is in Drs Taybi and Lachman’s
excellent book, Radiology of Syndromes, Metabolic Disorders, and Skeletal
Dysplasias.3 Besides providing a comprehensive list of syndromes, this book
also has a logical layout, much like a good cookbook. Each of the more than
1900 “recipes” in this book lists the following: name of the disorder, common
synonyms, the mode of inheritance, frequency of occurrence, clinical findings,
radiographic findings, a differential diagnosis (if any), and a list of pertinent
references, including the original description(s) of the syndrome. Unfortunately,
this book is currently out of print and used copies are currently quite expensive.
If you do not have access to a copy of Taybi and Lachman’s book, you can go
online to a wonderful Web site known as the OMIM database. This site is a
continually updated textbook on congenital disorders of all types. As of February
10, 2017, they list 23 916 entries.4 Another excellent online resource is Orphanet
—the portal for rare diseases and orphan drugs.7 This site is led by a consortium
of about 40 countries and is coordinated by the French INSERM team. Their
motto: “Rare diseases are rare, but rare disease patients are numerous.” As of
February 2017, the Orphanet site contains information on 5856 diseases. They
have also created an excellent Orphanet app for both iPhone and Android
devices. Another free resource is a book written by me and one of my pediatric
radiology colleagues titled The Little Book of Skeletal Dysplasias.8 Besides
chapters on several common dysplasias, it has an interactive atlas in its final
chapter that we informally call “The Amazing Skeletron.” This allows one to
quickly flip through multiple images of a given body part and find a dysplasia
that most closely matches one’s own patient. If you cannot find the answer you
need in Taybi and Lachman or OMIM or Orphanet, you have done your best,
and it is probably now time to punt.
Step 5: Is It Time to Pass This on to a Real Expert?

If you have gotten this far without making a diagnosis, the answer is yes. The
next question is how do you find a true expert in dysplasia? If your town has a
local children’s hospital, that would be a great place to start. When a clinician
consulted me on the images in Figure 23.4, I was a bit nonplussed. I cannot tell
you how great it was to know the back line phone number for a colleague at
Seattle Children’s Hospital. He had no trouble recognizing this as an obvious
case of acrodysostosis, which was definitely not on my diagnostic radar.
If you do not have any local experts on speed dial, it is time to look online.
The Internet is a really big place, so here are a few places where you might start
your search:
1. Run a PubMed search on the disorder of interest and find out who has been
writing the most papers on that disorder. These are the real experts. The
PubMed citations usually list the institution where these experts work, often
with an e-mail address. The Web or an actual telephone directory may turn
up other contact information for them. Hopefully, there will be an actual
dysplasia expert in a town, state, or country near yours.
2. International Skeletal Dysplasia Registry9—another fine resource based at
UCLA. This group works with families, physicians, and researchers from
around the world to classify skeletal disorders radiographically,
histologically, and genetically.
3. European Skeletal Dysplasia Network10—an excellent resource for
physicians and patients based in Europe.
4. Orphanet has an online search engine7 for finding institutions or individuals
who have experience with dysplasia.
5. The NIH Office of Rare Disease Research11 has additional information on
rare diseases.
6. The National Organization for Rare Diseases12 has a disease database and
many educational materials for patients, families, clinicians, and researchers.
•
FIGURE 23.4 A 7-year-old boy with acrodysostosis. A, Lateral skull radiograph
shows prognathism and premature closure of the coronal suture. B, Bilateral hand
radiograph shows acroosteolysis.
PART 2: RADIOLOGY OF BONE DYSPLASIA IN ADULTS
Achondroplasia
Dwarfism is the condition of being disproportionately undersized. Skeletal
dysplasias with dwarfism are legion. Dozens of specific types are listed in the
2010 revision of the Nosology and Classification of Genetic Skeletal
Disorders.13
However, do not despair. Most types of dwarfism are very rare and quite a
few are lethal and will not be needing radiographs (such as thanatophoric
dwarfism, the most common form), none are reversible, and most are not defined
on a radiologic basis. The distinction among the dysplasias with dwarfism often
requires detailed genetic, biochemical, histochemical, and histopathologic
analysis. The bottom line is that unless you are going into high-risk OB
ultrasound or a pediatric radiology practice at a major, big-city children’s
hospital, you can save space in your brain by learning about something else.
Of the nonlethal types of dwarfism where patients survive to adulthood, often
with normal life spans, the only relatively common types are achondroplasia and
pseudoachondroplasia.
Classic achondroplasia is the most common form of short-limbed dwarfism.14
It is a common autosomal dominant disorder and is compatible with a long life
span. The homozygous form, born of 2 parents with this common heterozygous
form, is quite rare and quite lethal. However, most cases of achondroplasia are
sporadic, due to new mutations, rather than inherited. The estimated prevalence
is about 1 to 9/100 000.15 Achondroplasia is due to mutations in the fibroblast
growth factor receptor 3 (FGFR3) gene, encoding a transmembrane receptor that
is important in regulating linear bone growth.
•
FIGURE 23.5 Achondroplasia in an adult. A and B, The right and left femurs are
short and thick.
The very name of this syndrome suggests that the primary problem here is a
generalized defect in endochondral bone formation.16 Once you know this, you
can predict a lot of the findings seen in these patients. Most of the appendicular
skeleton is formed by and grows in size by endochondral bone formation.
Therefore, we can accurately predict that the long bones (and therefore the
patient) will be short. The result is a symmetric short-limbed dwarfism in which
the proximal segments of the extremities are disproportionately short (rhizomelic
micromelia) (Figures 23.5 and 23.6). Because periosteal bone growth is
unaffected, the shafts of the long bones are of normal diameter. The fingers are
short and stubby.
The characteristic shape of the skull and face in achondroplasia is also a
logical extension of these principles. The calvarium is modeled on membranous
bone, and its eventual size is merely a reflection of brain size. These people have
normal brains that are of normal size, so their calvaria are likewise of normal
size. However, the face and skull base come from endochondral bone and end up
relatively small, in comparison to the skull.
•
FIGURE 23.6 Pelvis of an adult with achondroplasia, demonstrating characteristic
disproportionately shortened shape of the pelvis, short femoral necks, and previous
lumbar decompression and fusion for spinal stenosis.
•
FIGURE 23.7 Achondroplasia in adult with spinal stenosis in the lumbar region.
Laminectomy has been performed at multiple levels.
The foramina of the skull base and spine and the spinal canal are often small,
which may lead to prominent neurologic problems and spinal stenosis17 (Figure
23.7). There is an exaggerated lumbar lordosis with prominent buttocks. These
abnormalities are usually evident at birth and become more apparent with age.
In the popular television series Game of Thrones, the fictional character
Tyrion Lannister (played by the actor Peter Dinklage), a member of the ruling
family who survives dizzying reversals of fortune, has achondroplasia (as does
the actor). The physical manifestations of achondroplasia are visible on the
screen, although there are apparently no X-rays in this particular fantasy world.
•
FIGURE 23.8 Pelvis of a 27-year-old man with pseudoachondroplasia, showing
marked flattening and deformation of his femoral heads. The obturator rings and
proximal femurs are also somewhat dysplastic.
Pseudoachondroplasia
Pseudoachondroplasia is roughly half as common as classic achondroplasia.18 It
is characterized by a normal face and skull with short-limbed, short-trunked
dwarfism. It is caused by a mutation of the cartilage oligomeric matrix protein
(COMP) gene on chromosome 19. Joint laxity is common. The exact prevalence
of pseudoachondroplasia is unknown, but it is estimated to occur in about
1/30 000 individuals.19
Pseudoachondroplasia is not clinically or radiologically evident until early
childhood (age 2-4 years). It therefore does not enter into the differential
diagnosis of the newborn short-limbed dwarfs.20 The chief features that
differentiate pseudoachondroplasia from classic achondroplasia are18 as follows:
(1) late discovery of the abnormality, (2) absence of clinical or radiologic
abnormalities in the face and skull, and (3) radiologic findings of gross
irregularities in the epiphyseal-metaphyseal areas with fragmentation of the
epiphyseal ossification centers. These patients are intellectually normal and adult
height varies between 82 and 130 cm.18 The main disability is due to secondary
osteoarthrosis of the hip and knee (Figure 23.8). Corrective osteotomy for gross
deformities may be done after skeletal maturity is reached. Replacement
arthroplasty may be appropriate in adults.
Dactyly
Anomalies of the fingers or toes may be sporadic or inherited and may be either
isolated or associated with a congenital syndrome. Individually, they are rare, but
when grouped together, they are not uncommon.
Syndactyly is congenital failure of segmentation of 2 or more digits. This
“fusion” may involve soft tissue or bone and may be either partial or complete
(Figure 23.9). The most common situation is a soft-tissue web between 2 fingers.
Clinodactyly is medial or lateral curvature of the digit (Figure 23.10). Common
as an isolated feature of the small finger, clinodactyly may also be associated
with various congenital syndromes. Polydactyly is the presence of
supernumerary digits, either partial (Figure 23.11) or complete (Figure 23.12).
Symphalangia is congenital fusion of one phalanx to another in the same digit,
presumably from failure of the intervening joint to develop (Figure 23.13).
Symphalangia is common in the fifth toes, a finding that generally has no
significance. Hyperphalangia is the presence of extra phalanges in the
longitudinal axis of a digit. It is seen almost exclusively as a triphalangeal
thumb. However, a triphalangeal thumb may be the result of surgery (Figure
23.14). Brachydactyly is the condition of relatively short fingers or toes and may
be the result of short metacarpals (Figure 23.15) or metatarsals, short phalanges,
or both. Brachydactyly may be acquired, isolated, or part of a congenital
syndrome.
•
FIGURE 23.9 Syndactyly of the fourth and fifth toes.
•
FIGURE 23.10 Clinodactyly in a patient with tricho-rhino-phalangeal syndrome.
•
FIGURE 23.11 Partial supernumerary digit between fourth and fifth rays, with
symphalangia between the supernumerary digit and the fifth toe.
•
FIGURE 23.12 Polydactyly of the foot shown on long-axis T1 MRI.
Macrodystrophia lipomatosa is a sporadic congenital form of localized

gigantism that typically affects 1 or more adjacent digits of a foot or hand
(Figure 23.16). There is unilateral dysplastic overgrowth of fibroadipose and
other mesenchymal tissues, including the bone. Overgrowth tends to be greatest
distally and volarly and stops at puberty. The radiographic appearance is
distinctive and should be distinguishable from other causes of macrodactyly such
as tumors or plexiform NF.21 The etiology is unknown, and cases are rare.
Enchondromatosis
Most enchondromas are solitary. However, some patients may have a syndrome
of multiple enchondromas, also known as Ollier disease. The estimated
prevalence of the disease is 1 in 100 000.22 Ollier disease is not hereditary. Ollier
disease usually involves the tubular bones of the arm or leg. Along with the
classic central expansile pattern seen with solitary enchondromas, one may also
see linear or columnar lucencies in the metaphyses, representing columns of
growing cartilage (Figures 23.17–23.19). The main significance of this disorder
is that some lesions will undergo malignant degeneration (5%-30%), usually to
chondrosarcoma. This likelihood is even higher (approaches 100%) when
multiple enchondromas are associated with soft-tissue hemangiomas (Maffucci
syndrome). These hemangiomas may contain phleboliths, making the diagnosis
possible on radiographs (Figure 23.20).
•
FIGURE 23.13 Symphalangism involving the lesser toes.
Marfan Syndrome
Marfan syndrome is an autosomal dominant disorder of connective tissue with a
high degree of clinical variability, primarily involving the eye, skeleton, and
cardiovascular system.23 It is a result of mutations of the FBN1 gene, located on
chromosome 15, which encodes for fibrillin-1, a major component of the
extracellular microfibrils. About one-quarter of affected individuals arise as new
mutations. The prevalence of the syndrome is estimated to be 7 to 17/100 000.24
•
FIGURE 23.14 Following the loss of the thumb in an accident, the hand was
reconstructed by transplanting the second toe to replace the thumb.
•
FIGURE 23.15 Bilateral brachydactyly (multiple short metacarpals) in a patient with
pseudohypoparathyroidism.
•
FIGURE 23.16 An athletically active man with macrodystrophia lipomatosa, who is
asymptomatic except for trouble fitting shoes. There is marked, dysplastic
enlargement of the first 3 toes, greatest distally.
•
FIGURE 23.17 Multiple enchondromas in the hand of a patient with Ollier disease
(enchondromatosis).
•
FIGURE 23.18 Multiple enchondromas in the chest of a patient with Ollier disease
(enchondromatosis).
•
FIGURE 23.19 Multiple enchondromas in the pelvis and left femur of a patient with
Ollier disease (enchondromatosis).
FIGURE 23.20 • Maffucci syndrome with multiple enchondromas in the first
metacarpal and thumb and phleboliths in hemangiomas over the ulna and fifth
metacarpal.
Clinical features include increased height and disproportionately long limbs

and digits (arachnodactyly) (Figure 23.21). Other common skeletal findings
include scoliosis (Figure 23.22) and hypermobile joints. Common ocular
abnormalities include bilateral ectopia lentis, myopia, and retinal detachments.
Associated cardiac abnormalities lead to a shortened life expectancy for these
patients, approximately 32 years for untreated patients.24 These abnormalities
include cystic medial necrosis of the aorta or pulmonary arteries (leading to
dissection or rupture), aortic and mitral insufficiency, and septal defects. These
cardiovascular abnormalities are the predominant cause of death in more than
90% of cases.
Molecular genetic testing for mutations of the FBN1 gene can now be
performed. The sensitivity of such testing is substantial but remains incomplete
for unknown reasons.23 The diagnosis is therefore made clinically, based on
family history and the observation of characteristic findings in multiple organ
systems using the revised Ghent nosology, where ectopia lentis and aortic
aneurysm are given special significance in the diagnosis. In the absence of any
family history, the presence of these 2 manifestations is sufficient for the
unequivocal diagnosis of Marfan syndrome.25
Multiple Hereditary Exostoses

Osteochondromas usually have an absolutely pathognomonic appearance. The
key word here is “continuity.” The cortex and medullary space of normal bone
flows continuously into that of the osteochondroma (Figure 23.23).
•
FIGURE 23.21 Arachnodactyly in Marfan syndrome.
•
FIGURE 23.22 Severe thoracolumbar scoliosis in a patient with Marfan syndrome
shown on surface-rendered 3D CT.
Multiple hereditary exostosis (MHE) syndrome is an autosomal dominant

disorder characterized by the development of benign tumors, multiple
osteochondromas (exostoses), growing outward from the metaphyses of long
bones. MHE is a genetically heterogeneous disorder and is associated with
mutations in the tumor suppressor genes EXT1 or EXT2. Prevalence is estimated
to be 1 in 50 000.22,26,27 Unfortunately, this syndrome is associated with an
increased likelihood (up to 10%, depending on which study one quotes) that 1 or
more of these osteochondromas will undergo malignant degeneration, usually to
a chondrosarcoma (Figure 23.24). Some patients without this syndrome will
occasionally develop 1 or more osteochondromas. The likelihood of malignant
degeneration is much lower with sporadic osteochondromas such as these. A
person with MHE has 1000 to 2500 times the risk of development of a
chondrosarcoma compared with a person who does not have the disorder, and
the lifetime risk of chondrosarcoma is about 1% to 2%.26
•
FIGURE 23.23 Multiple hereditary exostoses. Right knee radiograph shows multiple
pedunculated osteochondromas and dysplastic metaphyses.
FIGURE 23.24 • A patient with multiple hereditary exostoses and malignant
degeneration into chondrosarcoma. Lateral ankle radiograph demonstrates sessile
osteochondromas in the distal tibia. There is also a large soft-tissue mass with
multiple speckled and rings-and-arcs calcifications, consistent with chondrosarcoma.
•
FIGURE 23.25 Multiple hereditary exostoses. Anteroposterior pelvis radiograph
shows multiple sessile osteochondromas, marked dysplasia of the proximal femurs,
and chronic dislocation of the right hip.
As it turns out, this fascinating syndrome has many points of similarity with
some of the colonic polyposis syndromes. For example, the lesions may be
pedunculated or sessile, they may be single or too numerous to count, and they
may undergo malignant degeneration. The trick, then, in both syndromes, is
determining which folks have the syndrome and which ones do not. The answer
in both cases is that one looks for evidence that the process is a systemic
disorder and not just a focal, sporadic lesion. In the polyposis syndromes, one
may look for other manifestations, such as associated osteomas (Gardner
syndrome) or buccal pigmentation (Peutz-Jeghers syndrome). With MHE
syndrome, one looks for other dysplastic bones. A common place to find this is
in the femoral and humeral necks. Patients with MHE generally have short, thick
necks in both anatomic sites. For this reason, after finding the first
osteochondroma, one of the first things I would like to see is a radiograph of the
patient’s hips (Figure 23.25).
You can explain a lot of things about osteochondromas if you consider them
to be an ectopic epiphysis. This means that they grow right along with the
normal epiphyses and stop growing when the plates close. They look just like
physes on radionuclide images in kids—hot until the plates close. These ectopic
growth plates also sometimes will cause the bone to grow into strange shapes:
too short, too long, or too curved. About 75% of affected individuals have a
clinically recognizable osseous deformity, most commonly involving the forearm
(50%)26 (Figure 23.26).
Once you have diagnosed this disorder, you must make sure that the patient
and their caregiver know the significance of their disorder and that they are now
on a lifelong surveillance program. Any development of pain or growth in an
osteochondroma after the plates have closed should be looked upon with
suspicion for malignant degeneration. Follow-up imaging studies may include
both radiographs and radionuclide images.
Neurofibromatosis
NF is one of the heritable phakomatoses, characterized by multisystem
involvement of hamartomas involving all 3 germ cell layers. This disorder is
seen in approximately 1 out of 3000 births. It is usually inherited as an
autosomal dominant disorder, but there is a high rate of new mutations. There
are multiple subtypes of NF, but 2 distinct forms of NF are most commonly
noted: the peripheral form (NF1, also called von Recklinghausen syndrome, seen
in 90% of patients with neurofibromatosis) and the central form (NF2, the form
characterized by acoustic neurofibromatosis).
There are many manifestations of NF1, and virtually every part of the body
may be affected. Café au lait spots may be seen, classically with smooth margins
like the “coast of California.” The skeleton is affected in about 80% of patients.
The most dramatic findings are the multiple neurofibromas seen throughout the
body, especially in the peripheral, cranial, or spinal nerves and in the
subcutaneous tissue (Figures 23.27 and 23.28). Fifty percent of patients with NF
may develop kyphoscoliosis, usually in the high thoracic spine. Although the
scoliosis may be gently curving and identical to idiopathic scoliosis,
occasionally a sharply angulated dysplastic thoracic kyphoscoliosis is present
and is virtually diagnostic. Scoliosis may progress rapidly and lead to paraplegia.
Mesodermal dysplasia may result in focally abnormal or deficient bone
formation. Other skeletal manifestations include posterior scalloping of vertebral
bodies, hemihypertrophy, bowing, pathologic fracture, pseudoarthrosis, and
defective fracture healing. The tibia is a characteristic site for pseudoarthrosis
(Figure 23.29); repeated failures to heal after treatment often lead to amputation.
Neurofibromas may erode adjacent bones, such as the spinal neural foramina,
and present as soft-tissue masses.
Osteogenesis Imperfecta
Osteogenesis imperfecta is a group of inborn connective tissue disorders due to
mutations of the COL1A1/2 gene. It is characterized by radiographically
decreased bone density. The underlying problem is one of abnormal collagen
synthesis, in which a variety of different molecular defects in collagen produces
a continuous spectrum of phenotypes. The prevalence of osteogenesis imperfecta
is about 1 per 20 000 to 60 000 live births. The condition is inherited in an
autosomal dominant manner, although many cases arise de novo. The proportion
of cases caused by a de novo COL1A1 or COL1A2 mutation varies by the
severity of disease, ranging from 60% in the milder forms to 100% in the most
severe forms.28
•
FIGURE 23.26 Multiple hereditary exostoses. Wrist radiograph shows multiple
sessile osteochondromas and marked dysplasia of the distal radius and ulna, with
prominent negative ulnar variance.
•
FIGURE 23.27 Bilateral plexiform neurofibromas (arrows) in a patient with NF1 (a
neurofibromatosis subtype).
•
FIGURE 23.28 Neurofibromatosis in an adult. A, Axial T1 MRI shows multiple
lobulated soft-tissue mass in and around the right buttock with dysplastic underlying
bone and muscle atrophy. B, Axial T2 MRI shows high signal within the masses.
In general, there are autosomal recessive severe forms that present at birth
and autosomal dominant forms that present later and have a mild course. The
condition ranges from severe, congenital involvement with multiple fractures in
utero and perinatal death to mild, late manifestations in adulthood. The severe
forms account for 10% of cases; the less severe forms account for the remaining
90%.
•
FIGURE 23.29 Neurofibromatosis with pseudoarthrosis (arrow) of the tibia in a
child. A telescoping rod has been placed for mechanical support, but the fracture has
not healed.
This generalized disorder of connective tissue is characterized by abnormal

maturation of collagen. It affects the skeleton, ligaments, skin, sclera, and teeth
with variable expression. The major clinical diagnostic triad is generalized
osteoporosis with skeletal fragility, blue sclera, and odontogenesis imperfecta.
Any 2 of these features suffice for the diagnosis. Other clinical features include
thin, translucent skin; hypermobile, lax peripheral joints; and deafness (fragile
otic bones).
Growth retardation occurs in most cases and may be marked to the point of
dwarfism in severe cases. This short stature is due to not only defects in collagen
synthesis but also the cumulative fracture deformities secondary to the fragile
bones.
The most common radiographic finding is that of generalized osteopenia
(Figures 23.30 and 23.31). Multiple fractures resulting from insignificant trauma
or normal muscle pull are also seen commonly and may result in considerable
deformity. Exuberant callus formation and pseudarthroses may also be seen.
Persistent Wormian bones may be seen in the skull.
Osteopetrosis
Osteopetrosis is a group of heritable diseases characterized by reduced bone
resorption from osteoclast failure. Many genetic defects may cause osteoclast
failure, each having different underlying biochemical and histopathologic
abnormalities. One form is associated with renal tubular acidosis and rickets.
The final common effect is that bone remodels incompletely or not at all.
Osteopetrosis manifests as 1 of the 3 major clinical groups: (1) infantile-
malignant autosomal recessive, which is fatal in childhood (in the absence of
effective therapy) with a prevalence around 1:250 00029; (2) intermediate
autosomal recessive, which appears during the first decade of life but does not
follow a malignant course; and (3) autosomal dominant, also known as Albers-
Schönberg disease or marble bones disease, with a prevalence of about
1/20 00029,30 and a normal life expectancy but many orthopedic problems.
•
FIGURE 23.30 Osteogenesis imperfecta in an adult. A and B, Anteroposterior
radiographs of the right and left knees show osteoporosis, bowing deformity, and
dysplastic epiphyses. There are intramedullary rods in both femurs and tibias. There
is an acute fracture of the right femur and a healing fracture of the left tibia and fibula.
The radiographic manifestations of osteopetrosis arise in a logical manner

from osteoclast failure. Without properly working osteoclasts, the whole bone
remodeling process will fare badly, leaving one with short, weak, and oddly
shaped bones. With abnormal osteoclasts, one might predict the following
abnormalities: (1) dense bones that break easily, (2) small or absent medullary
space, and (3) small neural foramina.
Osteopetrosis is rarely a diagnostic conundrum. The combination of
extremely dense bones with small medullary spaces (Figures 23.32–23.34) is
rarely mistaken for any other process, with the possible exception of a much
rarer disorder (prevalence = 1:1.7 million) called pycnodysostosis.31
•
FIGURE 23.31 Osteogenesis imperfecta in an adult. Markedly dysplastic pelvis with
femoral fractures of different ages.
FIGURE 23.32 • Osteopetrosis. This patient has very dense bones with tiny
medullary canals, as well as a transverse fracture of the radius. Marked bowing of the
radius suggests the presence of multiple previous fractures at this site.
The infantile variant has clinical manifestations that correlate with the lack of
marrow space development (anemia and thrombocytopenia) and the lack of
enlargement of bony remodeling (small cranial foramina result in cranial nerve
dysfunction, hydrocephalus, convulsions, and mental retardation). Radiographs
show uniformly dense bones with no medullary space, broadened metaphyses
(Erlenmeyer flask deformity), and bone-in-bone appearance at the tarsals,
carpals, phalanges, vertebrae, and iliac wings, and sandwich vertebrae.
Transverse insufficiency fractures occur often. Medical treatments involve high-
dose calcitriol to stimulate osteoclast differentiation and bone marrow
transplantation to provide monocytic osteoclast precursors.
•
FIGURE 23.33 Osteopetrosis. Radiograph of the shoulder shows dense bones
lacking a medullary space, including ribs, clavicle, scapula, and humerus. There is a
transverse fracture of the humeral shaft.
•
FIGURE 23.34 Osteopetrosis. Radiograph of pelvis shows dense bones lacking a
medullary space. There is an old hip fracture on the right and an acute hip fracture on
the left.
The intermediate and autosomal dominant (sometimes called tarda) forms

have mild manifestations that include anemia, cranial nerve palsies, and
orthopedic problems. The fragility of osteopetrotic bone and its inability to
remodel in response to stress result in repeated insufficiency fractures. Coxa
vara, long-bone bowing, hip and knee degenerative arthritis, and mandibular and
long-bone osteomyelitis may also occur. Even milder forms of osteopetrosis may
be asymptomatic and discovered incidentally on radiographs (Figures 23.35 and
23.36).
Osteopoikilosis
Osteopoikilosis (spotted bones, osteopathia condensans disseminata) is an
autosomal dominant skeletal dysplasia likely due to a loss-of-function mutation
in the LEMD3 gene.32 It is characterized by a symmetric but unequal distribution
of multiple hyperostotic areas in different parts of the skeleton. Osteopoikilosis
is relatively rare, with an estimated prevalence of 1/50 000.33 Symptoms are
generally absent or mild, and its discovery is frequently incidental. The
condition is defined by the presence of numerous small, well-defined,
homogeneous ovoid or circular foci of increased radiodensity clustered in
periarticular osseous regions. The distribution is symmetric, typically involving
the epiphyses and metaphyses of long bones, as well as the carpus, tarsus,
scapula, and pelvis (Figure 23.37). The lesions may increase or decrease in size
or number. They are histologically identical to bone islands but have no clinical
significance unless mistaken for other lesions.
Osteopathia Striata
Osteopathia striata with cranial sclerosis is a rare bone dysplasia characterized
by longitudinal striations of the metaphyses of the long bones and an estimated
prevalence of less than 1/1 000 000.34 The clinical presentation is highly variable
even within the same family, ranging from mild skeletal manifestations to
multisystem organ involvement, with sclerosis of the craniofacial bones,
macrocephaly, cleft palate, and hearing loss.
•
FIGURE 23.35 Osteopetrosis, incidental adult presentation. Note the sandwich
appearance of the vertebrae.
•
FIGURE 23.36 Osteopetrosis, incidental adult presentation. The pelvis shows
dense bones with bone-in-bone appearance in the iliac wings and vertebrae.
•
FIGURE 23.37 Osteopoikilosis. A, Anteroposterior hip radiograph shows multiple
small ovoid bony masses. B, Axial CT through both proximal femurs shows bilateral
small bony masses.
Osteopathia striata (also known as Voorhoeve disease) is associated with

mutations in the Wilms tumor gene on the X chromosome (WTX) and is X-
linked dominant. The condition is defined by the presence of linear, regular
bands of increased radiodensity extending from the metaphyses to the diaphyses
of tubular bones and the pelvis35,36 (Figure 23.38). Osteopathia striata is usually
bilateral, and discovery is often incidental.
Melorheostosis
Melorheostosis is a rare, nonhereditary condition that presents in childhood with
extremity pain, limitation of motion, and intermittent joint swelling. The
estimated prevalence is of 1/1 100 000.37 Its etiology remains obscure, although
some evidence suggests that it may be associated with loss-of-function mutations
in the LEMD3 gene.32 Growth disturbances, soft-tissue involvement, and
increasing muscle contractures due to tendon and ligament shortening may result
in considerable deformity and disability. The condition is commonly limited to a
single limb, usually lower. Radiologically, there is extensive periosteal or
endosteal cortical hyperostosis with bony excrescences extending along the
length of the bone, giving it a wavy contour that has been likened to wax
dripping down a candle (Figure 23.39). Endosteal hyperostosis may fill the
medullary cavity (Figure 23.40). The radiologic appearance is characteristic, and
the bony excrescences are histologically normal bone.
Madelung Deformity
Madelung deformity affects the distal forearm and results from a growth
disturbance at the ulnar-volar corner of the distal radial growth plate. As the
dorsal and radial portions of the radius continue to grow, there is a progressive
volar bowing of the distal radius and ulnar sloping of its articular surface. The
ulna grows normally and ends up longer than the radius, with an absent or
dysplastic distal radioulnar joint. Various bone dysplasias are associated with not
only Madelung deformity, particularly Léri-Weill dyschondrosteosis (Figure
23.41), but also multiple hereditary exostoses, Ollier disease, achondroplasia,
and others. A genetic basis has been established in some cases. There is a wide
range in severity, and patients may present as children or adults. There is a 4:1
female predominance. Premature closure of the ulnar-volar portion of the growth
plate during childhood from trauma, infection, or other cause may also result in a
similar deformity. The treatment is surgical correction and sometimes distal
radioulnar joint arthroplasty.
•
FIGURE 23.38 Osteopathia striata involving the tibia and talus. These findings were
discovered incidentally during evaluation of the distal fibular fracture.
•
FIGURE 23.39 Melorheostosis involving the fourth and fifth rays of the hand.
•
FIGURE 23.40 Melorheostosis involving the foot shown on axial CT.
•
FIGURE 23.41 Madelung deformity. A and B, Posteroanterior and lateral wrist
radiographs show dysplastic ulnar aspect of the distal radius with separation of the
distal ulna.
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Review of the roentgen manifestations. Am J Roentgenol Radium Ther Nucl Med. 1973;118(2):450–455.
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Clinical, genetic and radiologic considerations. Clin Pediatr (Phila). 1980;19(5):369–373.
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Expert=2485. Accessed February 12, 2017.
1. Which condition is most closely associated with spinal stenosis?

A. Achondroplasia
B. Melorheostosis
C. Osteogenesis imperfecta
D. Osteopetrosis
2. Which condition is most closely associated with osteopenia?

A. Achondroplasia
B. Melorheostosis
D. Osteopetrosis
3. Which condition is most commonly associated with tall stature?

A. Achondroplasia
B. Osteogenesis imperfecta
C. Multiple hereditary exostoses
D. Marfan syndrome
4. Which condition has the radiologic appearance of multiple bone islands?

A. Melorheostosis
B. Osteopathia striata
C. Osteopoikilosis
D. Neurofibromatosis

1. A Achondroplasia is associated with spinal stenosis.
2. C Osteogenesis imperfecta is associated with osteopenia.
3. D Marfan syndrome is associated with tall stature; the other options are
associated with short stature.
4. C Osteopoikilosis has the appearance of multiple bone islands.
24
Osteoporosis and Abnormal Mineral
Metabolism
This chapter describes the radiology of osteoporosis and various other conditions
of abnormal mineral metabolism.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of osteoporosis and disorders of
mineral metabolism, the learner will be able to
4. summarize relevant concepts and knowledge for the following topics: primary osteoporosis,
bone mineral densitometry, secondary osteoporosis, acute osteoporosis, transient regional
osteoporosis, regional migratory osteoporosis, hyperparathyroidism, vitamin D physiology and
function, vitamin D deficiency, and renal osteodystrophy.
OSTEOPOROSIS
Osteoporosis is the most common metabolic bone disease. Osteoporosis is
characterized by generalized loss of mass from otherwise normal bone. This loss
of bone substance results in microarchitectural deterioration of the trabecular
structure, increased bone fragility, and increased risk of fracture.1,2 Osteoporosis
may be considered to be primary or secondary. Primary osteoporosis, also called
involutional osteoporosis, is idiopathic in etiology. Secondary osteoporosis has a
known, underlying etiology.
Primary Osteoporosis (Involutional Osteoporosis)

More than 95% of adults with osteoporosis have involutional osteoporosis (also
called idiopathic or primary osteoporosis). There are 2 main clinical types: (1)
postmenopausal and (2) senile or age-related. Postmenopausal osteoporosis is
characterized by accelerated bone loss, mainly trabecular, and is caused by
factors related to menopause. Age-related osteoporosis is characterized by
slowly progressive bone loss, mainly cortical, and is caused by factors related to
aging. The pathogenesis of osteoporosis is incompletely understood; it seems to
involve not only excessive bone resorption but also impaired bone formation.3
Deteriorating bone strength results in increased vulnerability to traumatic and
fatigue fractures. Most fractures of the spine, proximal femur, and distal radius
in adults older than 50 years are associated with osteoporosis. In postmenopausal
osteoporosis, vertebral crush fractures and distal radius fractures are the most
common; in age-related osteoporosis, multiple vertebral wedge fractures and hip
fractures are the most common. Fractures and the resulting loss of function is the
major cause of morbidity and mortality in osteoporosis.
The prevalence of involutional osteoporosis in the United States is estimated
at 28 million or approximately 10% of the entire population. Risk factors for
developing involutional osteoporosis include advancing age; female gender;
white or Asian race; family history; thin, small bones; menopause; low dietary
calcium; low dietary vitamin D; excessive alcohol, caffeine, and salt; smoking;
and sedentary lifestyle. As the proportion and absolute numbers of the
population older than 50 years in the United States increase, the prevalence of
involutional osteoporosis may be expected to increase substantially.
The radiographic hallmark of osteoporosis is osteopenia, the increased
radiolucency of bone. However, osteopenia may not be recognizable on
radiographs until 30% to 50% of the bone mineral has been lost. A coarsened
trabecular pattern results from the loss of smaller trabeculae, making the
remaining ones more prominent. Linear, bandlike, or spotty radiolucent areas
may also be seen. Cortical thinning can be a generalized, uniform, slowly
progressive process (Figure 24.1).
Cortical bone loss may also be manifested by scalloped, endosteal erosions,
intracortical radiolucent areas or striations (intracortical tunneling), or
subperiosteal erosions. Vertebral deformities are related to insufficiency fractures
of the end plates. These can have the form of biconcave depressions of
contiguous superior and inferior end plates (so-called fish or codfish vertebrae,
named for their resemblance to vertebrae in codfish), anterior wedge fractures,
crush fractures of entire vertebral bodies, and increased thoracic kyphosis
(dowager’s hump) (Figures 24.2 and 24.3). The net result is progressive loss of
stature.
•
FIGURE 24.1 Osteoporosis of the hip with thin cortex and loss of trabecular bone in
the neck.
Bone Mineral Densitometry

Bone mineral densitometry is the best noninvasive method for the diagnosis of
osteoporosis in asymptomatic patients. Densitometry may also be used to
estimate the risk of fracture and monitor patients receiving therapy for
osteoporosis. The availability of effective therapies for osteoporosis—including
estrogen, bisphosphonates, and other pharmacologic agents—has increased the
usefulness of screening patients with various risk factors. The absolute amount
of bone mineral is predictive of fracture risk, making its accurate and precise
measurement important. Dual-energy X-ray absorptiometry (DXA) uses a dual-
energy X-ray source to measure the bone mineral density (BMD) of the lumbar
spine, proximal femur, or distal radius.
DXA works on the physical principle that bone mineral (predominantly
calcium) and soft tissue (predominantly fat and water) attenuate X-rays of high
and low energy to different degrees. By measuring the differential absorption of
X-rays of high and low energy, the absorption due to bone mineral alone can be
determined, and from that, the absolute amount of bone mineral in the path of
the X-rays can be calculated. Measuring BMD at the spine and proximal femur
(central measurement) is considered more useful clinically than measuring BMD
in the extremities (peripheral measurement). DXA provides measurements that
reflect the BMD of trabecular and cortical bone together.
Clinical interpretation of DXA results is based on population statistics. An
individual’s BMD measurement from DXA is compared with those of normal
populations.4 The consensus criteria used for clinical diagnosis are those of the
World Health Organization (WHO) (Table 24.1). An individual’s BMD is
compared with those of a population of normal, young adults to derive a T-score.
The T-score is the number of standard deviations from the reference population’s
mean, so that a T-score of −2.0 would be 2 standard deviations below the mean
of the young, normal population. The diagnosis of osteopenia is defined as a T-
score of less than −1.0 but greater than −2.5. Osteoporosis is defined as a T-score
of less than −2.5. The diagnosis of established osteoporosis is defined as
fractures and a T-score of less than −2.5. The comparison of an individual’s
BMD to an age-matched population (the Z-score) is not used in the WHO
criteria. There is significant controversy regarding the particular normal, young
adult populations on whom the T-scores are based with regard to sample size,
gender, and race. The use of the terms osteopenia and osteoporosis may also lead
to confusion unless the context is clear; when these terms are used in
conjunction with DXA, they should only refer to diagnoses according to WHO
criteria.
•
FIGURE 24.2 Osteoporosis in the spine with central endplate depressions of the
vertebral bodies at multiple levels.
•
FIGURE 24.3 Osteoporosis with multiple anterior wedge fractures in the thoracic
spine.
Table 24.1 WHO DIAGNOSTIC CRITERIA FOR INVOLUTIONAL OSTEOPOROSIS
Diagnosis T-Score
Normal −1.0 or higher
Osteopenia Less than −1.0 but greater than −2.5
Osteoporosis Less than −2.5 but without fractures
Established osteoporosis Less than −2.5 with fractures
•
FIGURE 24.4 Dual-energy X-ray absorptiometry of the lumbar spine showing
osteoporosis. A, Image shows regions of interest. B, Graphic shows bone mineral
density (BMD) relative to young-adult and age-matched reference populations. The T-
score was −3.3, diagnostic of osteoporosis.
In current practice, the DXA diagnosis of osteopenia and osteoporosis is

based on BMD measurements of the lumbar spine and the proximal femur. In the
spine, the frontal projection is used, and, ideally, an average of L1 through L4 is
used to obtain the T-score (Figure 24.4). If it is not possible to use L1 through
L4, any 2 or 3 consecutive L1 through L4 vertebrae can be used. The use of a
single vertebra is considered unreliable. In the hip, a region of the femoral neck
is used (Figure 24.5).
•
FIGURE 24.5 Dual-energy X-ray absorptiometry of the hips showing osteopenia. A,
Image shows regions of interest. B, Graphic shows bone mineral density (BMD)
relative to young-adult and age-matched reference populations. The T-score on the
right was −2.0, and the T-score on the left was −2.2, both diagnostic of osteopenia.
The DXA report typically includes a description of the basis of the

measurement, the T-score, the relative fracture risk associated with the T-score,
and the diagnosis according to WHO criteria. Because DXA is a projection
technique that measures the sum of the bone mineral between the X-ray source
and the detector, disease or postsurgical conditions that increase or decrease the
attenuation of the X-rays may compromise accuracy (Figure 24.6).
The most common condition leading to spurious BMD measurements (Tables
24.2 and 24.3) is degenerative spine disease, in which sclerosis and osteophytes
increase the BMD measurement. Similarly, diffuse idiopathic skeletal
hyperostosis may increase BMD measurement. Other common conditions that
affect DXA measurements include compression fractures, laminectomy, metal
artifacts and bone graft from spine fusion, focal sclerotic lesions such as blastic
metastases or Paget disease, and focal lytic lesions such as lytic metastases or
multiple myeloma. Similar conditions may affect DXA measurements of BMD
at the hip. Problematic anatomic regions with artifact-causing conditions should
be excluded from measurements.
Secondary Osteoporosis
Secondary osteoporosis is the loss of bone mass from otherwise normal bone as
a result of a known cause. Secondary osteoporosis may manifest acutely or
chronically, in a regional or systemic distribution. DXA and other methods for
determining BMD may be applied to patients with chronic, systemic, secondary
osteoporosis. Common causes of secondary osteoporosis are listed in Table 24.4.
More detailed descriptions of these conditions may be found in the appropriate
portions of this book.
Acute, Transient, Regional, and Migratory Osteoporosis

Acute osteoporosis accompanies fracture healing as a normal physiologic
response to hyperemia. It may also accompany immobilization and disuse; both
are common features of healing fractures, as well as conditions such as reflex
sympathetic dystrophy (also called complex regional pain syndrome). On
radiographs, acute osteoporosis may be recognized in cancellous bone by
subcortical resorption of trabeculae, resulting in subcortical lucency that
parallels the cortical surface. On CT, the bone resorption tends to appear patchier
(Figure 24.7).
•
FIGURE 24.6 Dual-energy X-ray absorptiometry artifacts. A, Degenerative spine
disease with endplate sclerosis and osteophytosis. B, Compression fracture at L1 and
degenerative changes at L4. C, Laminectomy and posterolateral fusion at L4. D,
Lumbar spine fusion with hardware.
Table 24.2 COMMON POTENTIAL CAUSES OF SPURIOUSLY INCREASED BONE

MINERAL DENSITY MEASUREMENT
Degenerative joint disease

Diffuse idiopathic skeletal hyperostosis
Spinal fusion
Orthopedic hardware
Compression fracture
Blastic metastases
Paget disease
Table 24.3 COMMON POTENTIAL CAUSES OF SPURIOUSLY DECREASED BONE

MINERAL DENSITY MEASUREMENT
Laminectomy
Lytic metastases
Multiple myeloma
Table 24.4 SOME CAUSES OF SECONDARY OSTEOPOROSIS IN ADULTS
Category Causes
Inherited Osteogenesis imperfecta
Homocystinuria
Marfan syndrome
Nutritional Malabsorption syndromes
Chronic liver disease
Alcoholism
Calcium deficiency
Endocrine Hypogonadism
Thyrotoxicosis
Hypercortisolism
Hyperparathyroidism
Drugs Corticosteroids
Phenobarbital
Levothyroxine
Phenytoin
Other Multiple myeloma
Acromegaly
Mastocytosis
Transient regional osteoporosis typically presents with monoarticular joint

symptoms. It is characterized by a rapidly developing osteoporosis affecting
periarticular bone that is self-limited and reversible and has no definite inciting
event. There are 2 clinical syndromes that occur in adults, both more common in
men. Transient osteoporosis of the hip presents with the rapid onset of severe hip
pain without a precipitating event. It is usually unilateral, involving either the
right or left hip in men, or usually the left hip in women. The pain is self-limited
but aggravated by activity and regresses in 2 to 6 months without permanent
sequelae. Imaging may show a rapidly developing periarticular osteoporosis,
particularly in the femoral head, which returns to normal after the resolution of
symptoms. MRI shows diffuse edema and hip effusion but no infarction. Bone
scans show increased activity consistent with the osteoporosis. The condition is
thought to have a neurogenic origin, possibly related to reflex sympathetic
dystrophy.
•
FIGURE 24.7 Acute osteoporosis, associated with healing femoral shaft fracture,
demonstrated on CT.
•
FIGURE 24.8 Transient osteoporosis of the hip. Coronal T2 FS MRI shows
amorphous bone marrow edema (arrow) in the right proximal femur.
Regional migratory osteoporosis (Figure 24.8) usually involves the lower

extremities of adults. Local pain and swelling develop rapidly, last up to
9 months, and then disappear only to be followed by delayed involvement of
other anatomic regions months to years later. Within weeks of the onset of each
episode, periarticular osteoporosis is evident. This condition may begin as
transient osteoporosis of the hip and then recur in other regions.
DISEASES OF MINERAL METABOLISM

The skeleton is a metabolically active reservoir of calcium and phosphorus in the
extracellular space. These minerals are maintained in tiny hydroxyapatite
crystals that have in aggregate a vast surface area and are rapidly and freely
exchanged into the extracellular fluid space. When necessary, the skeleton gives
up calcium to maintain the correct serum levels. The ionic concentration of
calcium is generally determined by the renal glomerular filtration rate, tubular
reabsorption of calcium, and the formation and resorption of bone. The serum
calcium level is tightly controlled by parathyroid hormone and 1,25-dihydroxy
vitamin D. Calcium can be directly released from the hydroxyapatite crystal or
liberated by osteoclastic destruction of bone. Bone formation and destruction are
closely coupled in the healthy person.
Hyperparathyroidism
Hyperparathyroidism stimulates osteoclastic resorption of bone. The excess
parathyroid hormone can be a result of primary or secondary
hyperparathyroidism. Primary hyperparathyroidism results in hypercalcemia and
is caused by excess parathyroid hormone production from diffuse parathyroid
hyperplasia or autonomously functioning parathyroid adenomas (single or
multiple). Secondary hyperparathyroidism is a response to sustained
hypocalcemia that is typically caused by chronic renal failure or gastrointestinal
malabsorption. Patients with long-standing secondary hyperparathyroidism may
develop relatively autonomous parathyroid function or tertiary
hyperparathyroidism. Diagnosis of these disorders is made by clinical and
laboratory findings, including direct measurement of serum calcium and
parathyroid hormone levels.
Although radiographic changes may occur at many sites, they are best
detected and monitored in the hands. Skeletal surveys of the whole body are
generally unnecessary. Radiologic signs of hyperparathyroidism include bone
resorption, brown tumors, bone sclerosis, and chondrocalcinosis. Bone
resorption occurs at all surfaces, including subperiosteal, intracortical (along
Haversian systems), endosteal, trabecular, subchondral, and subligamentous
locations. Subperiosteal bone resorption is virtually diagnostic of
hyperparathyroidism. Seen best and most frequently along the radial aspect of
the phalanges of the hands, especially the middle phalanges of the index and
middle fingers, subperiosteal bone resorption may also be evident at the
phalangeal tufts (Figure 24.9).
Bone resorption at other surfaces is nonspecific. Subchondral bone resorption
may lead to articular disease (Figure 24.10). Brown tumors are focal areas of
bone resorption where the bone has been replaced by fibrous tissue and
osteoclasts (Figure 24.11). Brown tumors may have the appearance of
aggressive, focally destructive bone lesions such as metastases, but the
associated presence of other radiographic changes of hyperparathyroid bone
disease should clarify the situation. Brown tumors may be single or multiple in
number and central, eccentric, or cortical in location (Figures 24.12 and 24.13).
Brown tumors heal by ossification (Figure 24.14). Widespread sclerosis of bone
in hyperparathyroidism occurs by an uncertain mechanism and may be
prominent in the axial skeleton, especially the skull and spine. Widespread
sclerosis is common in secondary hyperparathyroidism. When the spine is
involved, horizontal bands of sclerosis in the vertebral bodies adjacent to the
vertebral end plates may result in a rugger jersey appearance (Figure 24.15).
•
FIGURE 24.9 Secondary hyperparathyroidism. Subperiosteal bone resorption is
evident throughout the hand and more advanced on the radial aspect.
•
FIGURE 24.10 Hyperparathyroidism with sacroiliac joint bone resorption. Axial CT
shows subchondral bone resorption and widening of the sacroiliac joints.
Chondrocalcinosis, or calcification of cartilage, is associated with the

combination of primary hyperparathyroidism and calcium pyrophosphate
dihydrate crystal deposition disease. This combination is found in 18% to 40%
of primary hyperparathyroidism cases.
•
FIGURE 24.11 Brown tumor in hyperparathyroidism. A, Anteroposterior radiograph
shows osteoporosis and destructive lesion in proximal humerus. B, CT shows mass
destroying cortex of anterior humerus.
•
FIGURE 24.12 Secondary hyperparathyroidism with brown tumors (arrows) and
bone resorption on CT.
Sometimes, the distinction between primary and secondary

hyperparathyroidism can be suggested. The following combination of findings is
highly suggestive of primary hyperparathyroidism: subperiosteal bone
resorption, bone resorption at other sites, bony sclerosis, and chondrocalcinosis.
In secondary hyperparathyroidism, there is an increased frequency of vascular
and soft-tissue calcification, more common and more widespread bone sclerosis,
and a decreased frequency of chondrocalcinosis. Secondary hyperparathyroidism
is common; primary hyperparathyroidism is uncommon.
OSTEOMALACIA AND RENAL OSTEODYSTROPHY

Osteomalacia is the adult manifestations of a systemic disease with deficient
calcification of osteoids. The final common pathway is the lack of available
calcium or phosphorus (or both) for mineralization of osteoid. In osteomalacia,
the predominant effect is on remodeling of mature bone. When osteomalacia
occurs in conjunction with chronic renal failure, the condition is called renal
osteodystrophy. The same condition in children, rickets, is beyond the scope of
this book.
Vitamin D Physiology and Function

When the skin is exposed to sunlight (specifically UVB, the same wavelengths
that cause sunburn), it converts cholesterol into cholecalciferol (vitamin D3).
However, any cholecalciferol produced by the skin or absorbed from food via
the gastrointestinal tract is biologically inactive. As cholecalciferol in the blood
circulates through the liver, it is metabolized (hydroxylated) into a more active
form, called calcidiol (Figure 24.16). As this calcidiol circulates through the
kidneys, it undergoes an additional hydroxylation to become the most active
metabolite: calcitriol.
One of the most important roles of vitamin D is to help maintain skeletal
calcium balance.5 It does this by (1) promoting intestinal absorption of calcium
and phosphorus, (2) exerting a direct effect on bone mineralization, and (3)
exerting a minor phosphaturic effect on the kidneys.
Vitamin D and parathormone both exert negative feedback on parathyroid
cells.6 Low levels of vitamin D and calcium reduce this negative feedback. The
parathyroid glands respond to this reduced feedback by excreting more
parathormone. This helps to explain why some patients with significant levels of
vitamin D deficiency can also develop secondary hyperparathyroidism.
Receptors for vitamin D are present in the small intestines and osteoblasts, as
well as the colon and many other cells and organs (such as activated T and B
lymphocytes, islet cells, brain, heart, skin, gonads, prostate, breast, and
mononuclear cells). Epidemiologic studies over the past 2 decades have
suggested important effects of vitamin D on the immune system, in preventing
certain cancers, and in the development of type 1 diabetes mellitus,
schizophrenia, and multiple sclerosis.7
•
FIGURE 24.13 Brown tumor of the proximal femur. A, Anteroposterior radiograph
shows a lytic lesion (arrow) in the intertrochanteric region of the proximal femur. B,
Coronal T1 FS MRI following gadolinium injection shows rim enhancement (arrow) in
this cystic lesion.
•
FIGURE 24.14 Healing brown tumors involving the pelvis and proximal femurs
(arrows).
Vitamin D Deficiency
It is relatively easy to obtain all of the vitamin D that one needs via a modest
amount of casual exposure to direct sunlight.8 Vitamin D is also easily absorbed
via the gastrointestinal tract from foods naturally rich in D (eg, salmon), D-
enriched foods (eg, milk), and vitamin supplements.
•
FIGURE 24.15 Secondary hyperparathyroidism. Osteosclerosis with greater density
at the end plates (rugger jersey spine).
Despite this, an alarmingly high prevalence of vitamin D deficiency has been

described in numerous segments of the world population, including healthy Irish
adolescents (36%),9 women with osteoarthritis undergoing total hip arthroplasty
(40%),10 patients undergoing orthopedic surgery (43%),11 American
postmenopausal women taking medication for osteoporosis (50%),12 black and
Hispanic adolescents in Boston (52%),13 and young girls in Beijing (89%).14 In
the United States, gastrointestinal malabsorption from a variety of etiologies is
the most common cause of rickets and osteomalacia.
FIGURE 24.16 • The metabolic pathway for vitamin D production. GI,
gastrointestinal.
Furthermore, residents of northern latitudes may not have sufficient direct

sunlight for most of the year, and southern residents may get insufficient sunlight
because of the use of protective clothing or sunscreen. Older skin (>age
70 years) does not produce vitamin D as effectively as younger skin. Skin
pigment, body weight, and residence at altitude may also affect the amount of
skin-produced vitamin D.15 Patients with cystic fibrosis,16 inflammatory bowel
disease,17 intestinal failure,18 long-term use of magnesium or aluminum-
containing antacids,19 or taking antiepileptic drugs20 may also have lower levels
of vitamin D. Vitamin D deficiency can also occasionally be seen in food
faddists, the institutionalized elderly, and patients on total parenteral nutrition.
Other causes include failure of enzymatic conversion of 25-hydroxy vitamin
D to its physiologically more active metabolite 1,25-dihydroxy vitamin D, end-
organ insensitivity to 1,25-dihydroxy vitamin D, genetic and acquired renal
tubular reabsorptive defects, and gastrointestinal malabsorption of dietary
calcium or phosphorus.
X-linked hypophosphatemic rickets was initially referred to as vitamin D
resistant rickets because of the lack of therapeutic response to vitamin D in
dosages that would cure nutritional rickets.21 It has since been recognized that
renal phosphate wasting is the principal pathophysiologic abnormality in these
patients. A combination of active vitamin D metabolites and balanced doses of
phosphate have resulted in partial correction of the skeletal lesions in these
patients.
Rickets and osteomalacia may occur in association with polyostotic fibrous
dysplasia and neurofibromatosis and may also be caused by long-term use of
anticonvulsant medications or aluminum-containing antacids.
A rare cause of osteomalacia is oncogenic osteomalacia (aka tumor-induced
osteomalacia), in which a mesenchymal tumor (aka phosphaturic mesenchymal
tumor) secretes a factor (“phosphatonin,” which is FGF2322 in many cases). This
factor acts on the renal tubule to inhibit vitamin D and to increase urine
phosphate loss.15
•
FIGURE 24.17 Osteomalacia with bowing deformity and Looser zones (arrows).
Symptoms are nonspecific and include fatigue, bone pain, and

musculoskeletal weakness. This very nonspecificity may make the diagnosis
elusive.23 The offending mesenchymal tumors are often small and can difficult
to locate, even with advanced imaging. If the causative neoplasm can be located
and completely resected, the prognosis is excellent, often with rapid and
complete reversal of all symptoms. If the tumor cannot be located or is
unresectable, the symptoms can be treated with supplemental phosphate and
active vitamin D.
In osteomalacia, the radiologic findings are more subtle than in rickets
because the adult skeleton is less metabolically active. Osteopenia is the
predominant appearance, and it may be indistinguishable from osteoporosis
unless Looser zones or bowing deformities are present (Figure 24.17).
Occasionally, the bone texture may be recognized as subtly coarsened. As in
osteoporosis, the risk of fractures from falls escalates with deteriorating bone
strength.
•
FIGURE 24.18 Renal osteodystrophy. Anteroposterior radiograph of the foot shows
a coarsened trabecular bone pattern, cortical thinning, osteopenia, and vascular
calcification.
Renal Osteodystrophy
In renal osteodystrophy, the skeletal abnormalities include the findings of rickets
or osteomalacia, secondary hyperparathyroidism, osteoporosis, and soft-tissue
and vascular calcifications (Figure 24.18). The extent of the abnormalities
depends on the severity and duration of disease. Advanced changes have become
uncommon as the management of renal failure has improved. Articular
conditions that are related to chronic renal failure include amyloidosis,
periarticular calcinosis (dialysis-related tumoral calcinosis), and hydroxyapatite
crystal synovitis.
References
1. Cummings SR, Melton LJ. Osteoporosis. I: epidemiology and outcomes of osteoporotic fractures.
Lancet. 2002;359(9319):1761–1767.
2. Siris ES, Miller PD, Barrett-Connor E, et al. Identification and fracture outcomes of undiagnosed low
bone mineral density in postmenopausal women: results from the National Osteoporosis Risk
Assessment. JAMA. 2001;286:2815–2822.
3. Duque G, Troen BR. Understanding the mechanisms of senile osteoporosis: new facts for a major
geriatric syndrome. J Am Geriatr Soc. 2008;56(5):935–941.
4. Theodorou DJ, Theodorou SJ. Dual-energy X-ray absorptiometry in clinical practice: application and
interpretation of scans beyond the numbers. Clin Imaging. 2002;26(1):43–49.
5. Weller M, Edeiken J, Hodes PJ. Renal osteodystrophy. Am J Roentgenol Radium Ther Nucl Med.
1968;104(2):354–363.
6. Rastogi A, Bhadada SK, Bhansali A. Pseudoarthrosis and fracture: interaction between severe vitamin D
deficiency and primary hyperparathyroidism. Singapore Med J. 2013;54(11):e224–e227.
7. Misra M, Pacaud D, Petryk A, Collett-Solberg PF, Kappy M, Drug and Therapeutics Committee of the
Lawson Wilkins Pediatric Endocrine Society. Vitamin D deficiency in children and its management:
review of current knowledge and recommendations. Pediatrics. 2008;122(2):398–417.
8. Holick MF. Environmental factors that influence the cutaneous production of vitamin D. Am J Clin
Nutr. 1995;61(3 suppl):638S–645S.
9. Hill TR, Cotter AA, Mitchell S, et al. Vitamin D status and its determinants in adolescents from the
Northern Ireland Young Hearts 2000 cohort. Br J Nutr. 2008;99(5):1061–1067.
10. Glowacki J, Hurwitz S, Thornhill TS, Kelly M, LeBoff MS. Osteoporosis and vitamin-D deficiency
among postmenopausal women with osteoarthritis undergoing total hip arthroplasty. J Bone Joint Surg
Am. 2003;85-A(12):2371–2377.
11. Bogunovic L, Kim AD, Beamer BS, Nguyen J, Lane JM. Hypovitaminosis D in patients scheduled to
undergo orthopaedic surgery: a single-center analysis. J Bone Joint Surg Am. 2010;92(13):2300–2304.
12. Lips P, Hosking D, Lippuner K, et al. The prevalence of vitamin D inadequacy amongst women with
osteoporosis: an international epidemiological investigation. J Intern Med. 2006;260(3):245–254.
13. Gordon CM, DePeter KC, Feldman HA, Grace E, Emans SJ. Prevalence of vitamin D deficiency among
healthy adolescents. Arch Pediatr Adolesc Med. 2004;158(6):531–537.
14. Foo LH, Zhang Q, Zhu K, et al. Relationship between vitamin D status, body composition and physical
exercise of adolescent girls in Beijing. Osteoporos Int. 2009;20(3):417–425.
15. Ott SM. Vitamin D. Osteoporosis and bone physiology. Available online from:
http://courses.washington.edu/bonephys/opvitD.html. Accessed February 19, 2017.
16. Ott SM, Aitken ML. Osteoporosis in patients with cystic fibrosis. Clin Chest Med. 1998;19(3):555–567.
17. Issenman RM. Bone mineral metabolism in pediatric inflammatory bowel disease. Inflamm Bowel Dis.
1999;5(3):192–199.
18. Ubesie AC, Heubi JE, Kocoshis SA, et al. Vitamin D deficiency and low bone mineral density in
pediatric and young adult intestinal failure. J Pediatr Gastroenterol Nutr. 2013;57(3):372–376.
19. Sivas F, Günesen O, Ozoran K, Alemdaroğlu E. Osteomalacia from Mg-containing antacid: a case
report of bilateral hip fracture. Rheumatol Int. 2007;27(7):679–681 [Epub December 14, 2006].
20. Samaniego EA, Sheth RD. Bone consequences of epilepsy and antiepileptic medications. Semin Pediatr
Neurol. 2007;14(4):196–200.
21. Carpenter TO, Imel EA, Holm IA, Jan de Beur SM, Insogna KL. A clinician’s guide to X-linked
hypophosphatemia. J Bone Miner Res. 2011;26(7):1381–1388.
22. Wikipedia contributors. Fibroblast growth factor 23. Wikipedia, The Free Encyclopedia. June 3, 2016,
15:48 UTC. Available from: https://en.wikipedia.org/w/index.php?
title=Fibroblast\_growth\_factor\_23&oldid=723530016. Accessed February 19, 2017.
23. Hautmann AH, Hautmann MG, Kölbl O, Herr W, Fleck M. Tumor-induced osteomalacia: an up-to-date
review. Curr Rheumatol Rep. 2015;17(6):512.
1. Which radiologic finding is most closely associated with

hyperparathyroidism?
A. Diffuse periostitis
B. Subperiosteal bone resorption
C. Entheseal hyperostosis
D. Bone enlargement
2. Which radiologic finding is most closely associated with Paget disease?

A. Subperiosteal bone resorption
B. Diffuse periostitis
C. Entheseal hyperostosis
D. Bone enlargement
3. Which of the following conditions is most likely to affect the accuracy of DXA
in the lumbar spine?
A. Osteoporosis
B. Mild thoracic scoliosis
C. Diffuse idiopathic skeletal hyperostosis
D. Vitamin D deficiency
4. The rugger jersey appearance in the spine is most closely associated with
which condition?
A. Involutional osteoporosis
B. Regional migratory osteoporosis
C. Renal osteodystrophy
D. Vitamin D deficiency
1. B Subperiosteal bone resorption is characteristic of hyperparathyroidism.
2. D Bone enlargement is characteristic of Paget disease.
3. C The excess bone from diffuse idiopathic skeletal hyperostosis may affect
the accuracy of DXA.
4. C Rugger jersey spine is found in renal osteodystrophy.
25
Imaging of Systemic and Metabolic
Musculoskeletal Conditions
This chapter describes the radiology of many systemic conditions that have
musculoskeletal manifestations.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of systemic conditions affecting the
musculoskeletal system, the learner will be able to
4. summarize relevant concepts and knowledge for the following topics: hypercortisolism,
acromegaly, diabetes mellitus, Paget disease, sarcoidosis and hypertrophic osteoarthropathy,
and musculoskeletal toxicity from vitamin D, fluoride, vitamin A, bisphosphonates, statins,
gadolinium, fluoroquinolones, antiepileptic drugs, and highly active antiretroviral therapy.
HYPERCORTISOLISM
Hypercortisolism, or Cushing syndrome, is the clinical manifestation of
excessive amounts of glucocorticoids. Cushing disease refers to endogenous,
spontaneous hypercortisolism caused by an autonomously functioning pituitary
or adrenal lesion or by nonendocrine adrenocorticotropic hormone–producing
tumors. More commonly, hypercortisolism results from treatment with high
doses of synthetic cortisollike corticosteroids such as prednisone.
Hypercortisolism has 3 major effects on the musculoskeletal system:
osteoporosis, osteonecrosis, and muscle wasting.1,2 The combination of
osteoporosis of the axial skeleton and multifocal osteonecrosis of the
appendicular skeleton is typical of hypercortisolism. However, both osteoporosis
and osteonecrosis may have other causes.
Osteoporosis
Demineralization of bone is almost always present if hypercortisolism has been
present for a sufficient period. This bone loss can occur quite rapidly, reaching
6% to 12% in the first year.3 Glucocorticoids inhibit the absorption of calcium
from the intestine and increase renal calcium loss, leading to secondary
hyperparathyroidism.
Current evidence indicates that the pathogenesis of glucocorticoid-induced
bone disease also involves suppression of osteoblast and osteoclast precursors in
the bone marrow, increased apoptosis (a process of programmed cell death) of
osteoblasts and osteocytes, and prolongation of the lifespan of osteoclasts.4–6
The net result is continued generalized loss of bone that is prominent in the
spine, pelvis, ribs, and cranial vault. In addition to osteopenia, there may be
thinning of the cortex, loss of trabecular structure, intracortical tunneling,
vertebral central end-plate depressions, and insufficiency fractures. Once
steroids have been started, the relative risk of fracture increases rapidly,
escalating by as much as 75% within the first 3 months after beginning steroid
therapy.3
Besides the decrease in bone quantity, steroids have an even more adverse
effect on bone quality. When one compares patients with vertebral fractures due
to postmenopausal osteoporosis, glucocorticoid-treated patients with vertebral
fractures are about 10 years younger and have higher bone mineral density
(BMD) values but nevertheless suffer 2 to 12 times the risk of fracture.7
Insufficiency fractures characteristically heal with exuberant callus formation.
The vertebral end plates may have a sclerotic appearance that results from a
combination of insufficiency compressive microfractures and subsequent healing
(Figure 25.1).8 The osteoporosis of hypercortisolism is virtually
indistinguishable from that of involutional osteoporosis. This osteoporosis may
persist long after cortisol metabolism has been restored to normal or
corticosteroid treatment has ended.
Osteonecrosis
Focal regions of osteonecrosis may result from hypercortisolism, particularly
when the hypercortisolism results from exogenous corticosteroids. The classic
sites of involvement have been reported as the femoral and humeral heads, but
radiographically occult infarctions of the marrow in the shafts of long bones are
also common. The manifestations of corticosteroid-associated osteonecrosis may
be delayed, possibly appearing months or years after the treatment has begun or
ended. The mechanisms through which corticosteroid treatment results in focal
osteonecrosis have not yet been completely revealed, although an increase in
osteoblast and osteocyte apoptosis is believed to play an important role in its
pathogenesis.3 Severe secondary arthropathy may occur as a consequence of
osteonecrosis and mechanical collapse of subchondral bone; the resulting loss of
the bony support of the articular cartilage leads to excessive wear and
osteoarthropathy. This is a particularly common problem in the femoral head
(see chapter 27).
•
FIGURE 25.1 Hypercortisolism. Osteoporotic spine with advanced insufficiency
fractures of all the vertebral bodies.
Muscle Wasting
Muscle wasting is frequent in hypercortisolism and may vary in severity from
mild and virtually imperceptible to profound and obvious. In pronounced cases,
it may simulate muscular dystrophy.
ACROMEGALY
Clinical acromegaly is caused by excess growth hormone in adults. The
underlying cause in most cases is a pituitary adenoma that produces growth
hormone autonomously; however, extrapituitary growth hormone–secreting
tumors and central and peripheral tumors that secrete growth hormone–releasing
hormone may also cause acromegaly. Acromegaly has an equal incidence in men
and women and has a mean age at diagnosis of 40 and 45 years, respectively. In
younger patients, the onset tends to be rapid and often correlates with an
aggressive tumor; in older patients, the onset may be slow and insidious with
subtle changes occurring over a 5- to 10-year period. The clinical features of
acromegaly are distinctive and include acromegalic facies, enlargement of the
hands and feet, prognathism, and oily skin. Carpal tunnel syndrome,
degenerative joint disease, hypertension, Raynaud phenomenon, and diabetes
mellitus are commonly associated conditions. Many patients present with the
signs and symptoms of a pituitary or hypothalamic mass rather than those of
growth hormone excess. Definitive diagnosis is made by direct serum
measurements of hormone levels.
Growth hormone activates sites of bone remodeling and may increase bone
formation more than bone resorption. As a consequence, the bone mass may
actually be elevated, with thickened cortex and increased trabecular bone
volume. Periosteal bone formation at the insertions of tendons and ligaments and
periarticular hypertrophy at the insertions of joint capsules contribute to the
increase in skeletal mass.
Growth hormone increases chondrocytic activity and this leads to
hypertrophy of the hyaline articular cartilage. This thickened cartilage lacks the
normal biomechanical characteristics of articular cartilage and is vulnerable to
fissuring, ulceration, denudation, and degeneration of the articular surface.
Disordered joint mechanics and a brisk reparative process lead to widespread
osteophytic growths, subchondral cyst formation, and eventually to acromegalic
arthropathy. Superficially, the appearance of acromegalic arthropathy is similar
to that of osteoarthritis, but the joint spaces tend to be widened rather than
narrowed (Figure 25.2). When the process is so advanced that the cartilage has
completely disintegrated, the joint spaces are narrowed. The distribution of
involvement usually includes the large joints and the lumbosacral spine,
including sites normally spared by osteoarthritis such as the ankle and
glenohumeral joint. Calcinosis, skin hypertrophy, and nonspecific synovitis may
be associated.
Radiologic features of acromegaly include soft-tissue thickening; enlarged
sella with destructive changes; prominent facial bones and occipital
protuberance; enlarged, excessively pneumatized sinuses; increased vertebral
body and intervertebral disc height; posterior vertebral scalloping; exaggerated
thoracic kyphosis; hand and foot changes; and bony proliferation at entheses.8
Osteoporosis may occur late in the clinical course.
DIABETES MELLITUS
The prevalence of diabetes in the United States in 2012 was about 9.3% and has
been rising. Interrelated diabetic musculoskeletal complications include fragility
fractures; diabetic foot ulcers; serious infections including cellulitis,
osteomyelitis, and necrotizing soft-tissue infections; peripheral neuropathy;
neuropathic osteoarthropathy; peripheral vascular insufficiency; diabetic
myopathy; and various conditions related to renal failure. Fragility fractures in
type 2 diabetes are thought to be the result of impaired osteocyte health, poor
bone quality, and cortical porosity; BMD may be normal.9 Peripheral
arteriovenous fistulae may cause marked focal osteopenia or lysis of bone in the
involved limb. Diabetes is the most common cause of neuropathic
osteoarthropathy (see chapter 16). Certain soft-tissue conditions occur frequently
in diabetics, including frozen shoulder, calcific tendinitis or bursitis, Dupuytren
contracture, flexor tenosynovitis (trigger finger), and carpal tunnel syndrome.
Skeletal muscle infarction may occur as a result of vascular insufficiency,
particularly in the lower extremities. Acute muscle infarction may present as
pain, tenderness, or swelling, similar to infection. On MRI, the condition is
evident as diffuse enlargement and high T2 signal in the regions of involvement
(Figure 25.3); these findings are not specific.10,11 The diabetic foot is an
unfortunate but common confluence of diabetic morbidities affecting the foot
(see chapter 20).
•
FIGURE 25.2 Acromegaly with mature proliferative bone at the phalangeal tufts and
the insertions of the joint capsules. The soft tissues are thick, and the joint spaces are
wide. A, Posteroanterior radiograph. B, Lateral radiograph.
•
FIGURE 25.3 Diabetic myonecrosis. Coronal T2 FS MRI shows high signal in
regions of myonecrosis (arrow).
PAGET DISEASE
Paget disease (osteitis deformans) is a bone disease seen in middle-aged and
elderly individuals. It is characterized by excessive and abnormal remodeling of
bone.12 Usually asymptomatic, Paget disease has a prevalence of 3% in the adult
population older than 40 years. In most cases, involvement is polyostotic.
Although any bone may be involved, the preponderance of cases involves the
pelvis, spine, skull, femur, or tibia.
Current evidence suggests that the development of Paget disease is an
autosomal dominant trait with genetic heterogeneity and an as yet undetermined
relationship with paramyxoviral infection. The disease has active and quiescent
(inactive) phases. The active phase begins with a focus of excessive osteoclastic
activity that results in a localized area of osteolysis, where bone is replaced by
nonossified fibrovascular tissue. The demarcation between normal uninvolved
bone and the area of osteolysis is typically quite sharp. Subsequently, the areas
of osteolysis are filled in with pagetic bone, even as the osteoclastic activity
continues. Pagetic bone consists of layers of disorganized woven bone separated
by resorption cavities and nonossified fibrovascular tissue. Bone is formed both
endosteally and periosteally. The combination of osteoclastic and osteoblastic
activity results in rapid remodeling and turnover of bone. Eventually, for
unknown reasons, the osteoclastic activity moderates, and after the osteolytic
areas are filled with bone, the rate of bone turnover decreases. With the decrease
in turnover, the bone enters the quiescent phase of Paget disease. Focal areas of
pagetic bone may be replaced by islands of lamellar bone, but haversian systems
and remodeling along lines of stress do not occur. Slow endosteal and periosteal
apposition of bone may continue to thicken the cortex and enlarge the bone,
sometimes obscuring the marrow space on radiographs. The juxtaposition of
lamellar and woven bone yields a mosaic appearance on microscopy that is
diagnostic of Paget disease. Pagetic bone has a characteristic radiographic
appearance and evolution that is virtually pathognomonic.13
The progression of Paget disease may be seen radiographically in a long bone
(Figure 25.4). The disease begins typically at an epiphysis and slowly advances
at the rate of a few millimeters per year to involve the entire bone. The
advancing edge of osteolysis is radiolucent, with a sharp transition between
normal uninvolved bone and osteolysis. Behind the advancing osteolysis, pagetic
bone is found.
Pagetic bone has a coarsened trabecular appearance with diminished cortical
density. In the quiescent phase, the bone may become extremely dense, and the
overall size may be enlarged. Because remodeling along lines of stress does not
occur, insufficiency fractures and deformity are not uncommon. On MRI, the
thickening of cortex and trabeculae may be seen (Figure 25.5); however, the
marrow space remains normal.
•
FIGURE 25.4 Paget disease in a femur showing the lucent zone of osteolysis
(arrow) advancing distally into normal bone.
•
FIGURE 25.5 Paget disease at the knee. Coronal T1 MRI shows enlargement of
the distal femur and thickened trabeculae.
In vertebral bodies, the periphery (cortex) is involved first, widening the body
into a picture-frame appearance (Figure 25.6). Continued endosteal progression
results in a dense, sclerotic body. Characteristically, Paget disease involves the
entire vertebra, including the posterior elements (Figure 25.7).
In the skull, the common region of involvement is the cranial vault. The
osteolytic phase is called osteoporosis circumscripta and appears as a
geographic, well-demarcated region of bone resorption that may be mistaken for
a metastasis. Focal radiodensities occur as pagetic bone is formed. In the
quiescent phase, there is a radiodense cotton-wool appearance with a thickened
vault (typically 2-3 cm thick but often thicker). Basilar invagination of the skull
may follow because, despite its thickness, pagetic bone is weak. The
radionuclide bone scan can be used to identify all sites of involvement (Figure
25.8).
•
FIGURE 25.6 Paget disease with picture-frame vertebra appearance at L2. At L3,
there is also Paget disease with sclerosis and only mild enlargement of the bone. L4
is normal and not involved.
Clinical monitoring of Paget disease is accomplished by measuring serum

alkaline phosphatase levels and urinary hydroxyproline levels, both of which are
increased by osteoclastic activity. Although plain films can establish the initial
diagnosis, they change very slowly and are very insensitive for clinical
monitoring unless there is suspicion of a complication. Paget disease can be
treated with agents that arrest the osteolytic process: bisphosphonates, which
inhibit demineralization from the hydroxyapatite crystal, and calcitonin, which
inhibits bone resorption.
Complications include insufficiency fractures and sarcomatous degeneration.
Unless there is trauma, the insufficiency fractures are typically incomplete
horizontal lucencies at the lateral cortex (Figure 25.9). A complete fracture in the
absence of trauma should raise suspicion of an underlying sarcoma. Sarcomatous
degeneration of pagetic bone occurs rarely but is more likely in patients with
extensive disease. Osteolysis is the dominant radiographic feature (Figure
25.10).
The most important differential diagnosis for Paget disease is metastatic
disease. Metastatic disease may bear a superficial resemblance to Paget disease
but does not have the characteristic appearance of pagetic bone or the specific
organization of active and quiescent phases in the long bones. Sometimes, the
distinction is difficult to make. Although the distribution in the skeleton of Paget
disease is similar to the distribution of metastatic disease, involvement of the
ribs is rare in Paget disease and common in metastases. Discovery of a
metastasis within pagetic bone is a rare event.
•
FIGURE 25.7 Ivory vertebra from Paget disease. A, Lateral radiograph shows
sclerosis of the L1 vertebral body, obliterating the normal cortex and trabecular bone
pattern. The process extends from the vertebral body into the pedicles. B, Axial CT
shows increased density of the L1 vertebra with a disordered pattern of bone
deposition.
•
FIGURE 25.8 Paget disease in the femur. Radionuclide bone scan shows intense
activity in the regions involved by Paget disease.
•
FIGURE 25.9 Insufficiency fractures (arrows) in Paget disease.
DRUG EFFECTS
Drugs with teratogenic effects on the musculoskeletal system include
thalidomide, anticonvulsants, vitamin A and synthetic retinoids, alcohol, and
folic acid antagonists. Many drugs may have nonteratogenic effects on the
musculoskeletal system. Prostaglandin E, used in infants with ductus-dependent
cyanotic congenital heart disease, is associated with cortical hyperostosis.
Methotrexate in the setting of chemotherapy may cause osteoporosis and
scurvylike changes in bone. Other chemotherapeutic agents may be associated
with inflammatory myositis. Phenytoin and other anticonvulsants are associated
with rachitic or osteomalacic changes in bone.
Vitamin D Toxicity
Hypervitaminosis D is relatively rare and generally only occurs in patients who
ingest too much vitamin D in the form of supplements or in patients who are
given high doses of vitamin D in the treatment of renal failure. During UV
exposure from sunlight, vitamin D precursors produced in the skin reach an
equilibrium, and any further vitamin D produced is degraded.14
•
FIGURE 25.10 Paget sarcoma arising in the pelvis. A, Radiograph shows typical
findings of Paget disease in the right hemipelvis and hip, with a medial region of
destruction (arrow). B, Axial CT shows destructive mass (arrows) and typical pagetic
changes in the remaining portion of the ilium.
Hypervitaminosis D can result in anorexia, lethargy, growth retardation, bone

resorption, hypercalcemia, soft-tissue calcification, and death, possibly by
inducing a deficiency of vitamin K.15 Hypervitaminosis D may be accompanied
by fine deposits of metastatic calcification throughout the soft tissues or denser,
more globular deposits near joints (Figure 25.11).
•
FIGURE 25.11 Hypervitaminosis D due to voluntary ingestion of large quantities of
supplemental vitamin D. Large globular collections of amorphous calcification are
noted about the joints of the hand and wrist.
Periarticular calcinosis of the soft tissues is a nonspecific, but not uncommon

radiographic finding. The calcifications are often periarticular and may have a
lobular morphology with fluid-fluid levels. The most common cause for these
accumulations is chronic renal failure. However, the differential diagnosis also
includes numerous other possibilities,16 including connective tissue disease,
neoplasia, degenerative diseases such as calcium pyrophosphate or
hydroxyapatite deposition disease, and various hyperphosphatemic and
hypercalcemic states such as hypervitaminosis D. Because similar findings are
caused by renal osteodystrophy, hypervitaminosis D is usually not suspected
until the clinical condition improves without corresponding radiographic
improvement.
Fluoride
Fluoride compounds are commonly added to drinking water (0.7-1 ppm) and
toothpaste to prevent dental caries.17 Fluorosis occurs after chronic ingestion of
drinking water with endemic, excessive levels of fluoride (4 parts per million or
greater), excessive industrial exposure, or excessive use of fluoride-containing
medication. Radiographic findings include osteosclerosis and hyperostosis
involving the axial skeleton, periostitis and enthesopathy in the appendicular
skeleton, and dental abnormalities18 (Figure 25.12).
Fluorinated triazole antibiotics have been used in the past 2 decades for
antifungal prophylaxis in lung transplant recipients,19 a practice that has been
related to high serum fluoride levels and reversible skeletal disease,20,21
particularly in those with comorbid renal disease.22 The resulting periostitis can
manifest anywhere from 6 months to 8 years after treatment and can be quite
painful (Figure 25.13). These skeletal findings have primarily been reported with
voriconazole use. However, the serum fluorine excess and bone findings are not
seen with other fluorinated triazoles.23
FIGURE 25.12 • Skeletal fluorosis. Anteroposterior pelvis radiograph shows
symmetrically dense bones with cortical thickening.
Vitamin A and Analogues

Hypervitaminosis A can be caused by excessive vitamin supplementation in
infants and young children. However, a more common cause is the use of
vitamin A analogues to treat several skin diseases. High-dose vitamin A (retinol)
was shown to be an effective treatment for acne in 1949.24 However, these high
doses were known to cause skeletal hyperostosis, soft-tissue swelling, and
muscular pain.25 A search was therefore undertaken for less toxic analogues of
vitamin A. By 1972, all-trans-retinoic acid was being used to successfully treat
lamellar ichthyosis. By 1979, 13-cis-retinoic acid was shown to be highly
effective for acne.24 Shortly after this, high-dose 13-cis-retinoic acid was found
to cause diffuse idiopathic skeletal hyperostosis–like findings in the spine.26 By
1992, it was shown that even long-term very low doses of 13-cis-retinoic acid
could lead to these diffuse idiopathic skeletal hyperostosis–like lesions in the
spine.27 Retinoic acid can also cause hyperostosis at entheses elsewhere in the
skeleton28 (Figure 25.14).
Bisphosphonates
Bisphosphonates are used to treat osteoporosis and other conditions associated
with bone loss, such as multiple myeloma and lytic metastatic disease. These
agents interfere with osteoclast action and bone turnover and are associated with
increased BMD measurements and decreased osteoporotic fracture frequency.
Agents currently approved for use in the United States include alendronate,
ibandronate, risedronate, and zoledronic acid.29 Bisphosphonate use has resulted
in substantially reduced (39%-75%) fragility fracture rates in both clinical trials
and community practice in the spine, hips, and other skeletal sites.30–32 In some
patients taking bisphosphonates for osteoporosis, atypical femur fractures have
been reported in the subtrochanteric femoral shaft preceded by a characteristic
cortical bone formation along the lateral margins of the bones, sometimes with
an early fracture called the dreaded black line (Figure 25.15). These fractures are
worrisome because of their propensity to escalate to a completed fracture33
(Figure 25.16). Although completed fractures can be treated operatively, the
failure rate after surgery for bisphosphonate-related fractures ranges from 12%
to 46%, in contrast to the 1% failure rate noted in standard subtrochanteric
fractures.34,35 This marked increase in postoperative failure rate makes a strong
case for prophylactic intramedullary nail placement when these atypical fractures
are first discovered. These patients should continue to be closely monitored, as
21% of patients with 1 atypical femoral fracture will develop a contralateral
fracture.34 Alendronate, the most widely prescribed bisphosphonate drug, has an
estimated terminal elimination half-life of 10 years. Early estimates of the
incidence of atypical femur fractures have ranged from 2.3 to 5 fractures per
10 000 patient-years,36,37 as compared with a 30-fold higher incidence of typical
femur fractures in the same population.
•
FIGURE 25.13 Patient with acutely painful periostitis secondary to voriconazole
use. Marked exuberant periosteal reaction is noted in multiple fingers (arrows).
Statins
Statins are widely used medications for lowering serum lipids levels, with the
goal of reducing the risk of cardiovascular disease. Statins are associated with
varying degrees of muscle disease. Myalgias and weakness are the most
commonly reported musculoskeletal side effect and are seen in up to 21% of
patients.38 Myopathy (muscle pain with elevated creatine kinase levels) can be
seen in about 0.5% of patients. Rhabdomyolysis (widespread muscle damage)
has been reported in about 0.01% of subjects. Tendinopathy has also been
reported with statin therapy, with prevalence of about 1% to 4%.39
Nephrogenic Systemic Sclerosis

Nephrogenic systemic fibrosis (NSF), also known as nephrogenic fibrosing
dermopathy, occurs in patients with renal insufficiency who are exposed to
gadolinium-based contrast agents during the course of MRI.40 Cutaneous
changes of NSF include induration, thickening, hardening, and fibrotic nodules
and plaques that may lead to contractures (Figure 25.17). The nodules contain
proliferations of dermal fibroblasts and dendritic cells, thickened bundles of
collagen, elastic fibers, and deposits of mucin; gadolinium has been recovered in
such tissue samples. Fibrosis may involve other organs. Patients with NSF have
increased mortality and may have severe debility.
•
FIGURE 25.14 A 49-year-old woman with retinoic acid arthropathy. A, Lateral
radiograph of the thoracic spine shows flowing ossification of the anterior longitudinal
ligament of several thoracic vertebral bodies (arrows). The disk spaces and vertebral
body heights are normal. B, Anteroposterior radiographs of both elbows show
hyperostosis, especially involving the lateral humeral epicondyles at the origins of the
extensor tendons. Hyperostosis is also seen involving the sublime tubercles (arrows).
C, Anteroposterior radiograph of the pelvis shows enthesopathy at the iliolumbar
ligament insertions, anterior superior iliac spines (arrow), and hamstring tendon
attachments bilaterally. (Courtesy of Jonelle Petscavage, MD.)
Fluoroquinolone-Associated Tendinopathy
Fluoroquinolone antibiotics, such as levofloxacin and ciprofloxacin, are
prescribed for a variety of infections—most commonly of the urinary and
respiratory tract.41 Fluoroquinolone-induced tendinopathy was first reported in
1983,42 and 98 case reports of fluoroquinolone-associated tendinopathy had
accumulated by 2003.43 Although pefloxacin and ciprofloxacin are most
frequently implicated, tendon injury has been reported with most
fluoroquinolones. The prevalence of fluoroquinolone-induced tendon injury in
an otherwise healthy population is not well established, but reports suggest that
it is low, ranging from 0.14% to 0.4%.43 The Achilles tendon is most commonly
affected (Figure 25.18), with involvement of quadriceps, peroneus brevis,
extensor pollicis longus, long head of biceps, rotator cuff tendons, and other
tendons also reported.44 Healing occurs within 3 to 8 weeks after the drug is
stopped.41
Antiepileptic Drug–Related Bone Disease

Epilepsy is extremely common. The estimated worldwide prevalence of epilepsy
is about 0.4% to 1%,45 and an estimated 1% of the population is currently taking
an antiepileptic drug.46 The prevalence of bone disease in patients under
antiepileptic drug therapy is unknown but is estimated to be about 50%.46,47 For
the United States alone, this translates to about 1.5 million people with
antiepileptic drug–related bone disease.
One is not surprised to find an increased risk of falling in epileptic patients.
However, even when this is taken into consideration, the fracture risk from
antiepileptic drug is 2 to 4 times higher than that of the general population.46,48
Although the pathophysiology of antiepileptic drug–related bone disease remains
unclear, patients present with osteoporosis, osteomalacia, rickets, or all 3
disorders (Figure 25.19).
•
FIGURE 25.15 Bisphosphonate-related insufficiency fracture. Radiograph shows
periosteal bone formation along the lateral subtrochanteric femoral cortex, with a
dreaded black line (arrow).
It is worth asking what clinicians know and do about antiepileptic drug–

related bone disease. Unfortunately, several investigators have found “a striking
lack” of knowledge about antiepileptic drug–related bone problems among
pediatric or adult neurologists.49,50 These investigators found that only 28% to
41% of neurologists screened for antiepileptic drug–related bone disease, and
only 7% to 9% gave their patients basic prophylaxis with calcium or vitamin D.
Radiologists should therefore be mindful of the magnitude of this problem and
help to keep it on the radar of their clinical colleagues.
Highly Active Antiretroviral Therapy

Highly active antiretroviral therapy (HAART) is an extremely effective
treatment for human immunodeficiency virus (HIV) disease. Skeletal
complications of HAART include osteoporosis and osteonecrosis. Excess
fracture risk of 25% to 40% has been reported following HAART.51 Adjuvant
treatment of such osteoporosis includes switching to a different HAART,
supplemental vitamin D3, and bisphosphonate therapy.
Patients with HIV have an increased risk of osteonecrosis—up to 45 times
more than the general population.52,53 The risk of osteonecrosis in these patients
can further increase (up to 2-fold) with the addition of HAART.54 The
mechanisms for both of these increased risks remain unknown, but imaging
features are similar to osteonecrosis from other or unknown causes (see chapter
24).
SARCOIDOSIS
Sarcoidosis is a multisystem disease of unknown etiology characterized by the
presence of noncaseating granulomas. Although the predominant site of
involvement is the pulmonary system, sarcoidosis may involve the joints in
approximately 10% of cases. Sarcoidosis most often causes transient migratory
polyarticular arthralgias without radiographic findings. A chronic granulomatous
arthritis leading to chronic noncaseating granulomatous inflammation of the
synovium develops in only a few patients. Granulomas within or adjacent to the
bone may result in punched-out cortical erosions or central lytic lesions with
nonaggressive features within the medullary cavity. The fingers and toes are the
typical sites of involvement (Figures 25.20 and 25.21).55 The characteristic
appearance caused by the presence of multiple granulomatous lesions has been
described as lacelike.
•
FIGURE 25.16 Bisphosphonate-related insufficiency fracture. A, Radiograph shows
heaped-up periosteal bone formation (arrow) along the lateral subtrochanteric femoral
cortex, corresponding to an incomplete insufficiency fracture. B, Subsequent
radiograph (1 month later) shows catastrophic completion of the fracture, following
trivial trauma. C, Following open reduction and intramedullary rod placement, the
fracture can be seen to pass through the site of periosteal reaction (arrow).
•
FIGURE 25.17 Nephrogenic systemic sclerosis. A, Sagittal T1 MRI shows equinus
contracture of the foot. Fibrotic nodules (short arrow) are present in the plantar skin.
B, Sagittal T2 FS MRI shows edema in the skin (arrowheads) and muscle
compartments (long arrow).
•
FIGURE 25.18 Fluoroquinolone-induced Achilles tendinopathy. A, T1 MRI of the
right ankle obtained 18 days after the onset of symptoms demonstrates small foci of
increased signal in the medial-posterior margins of the Achilles tendon (arrow),
consistent with a small partial-width tear. B, T1 MRI of the left ankle shows a similar
small partial-width tear (arrow).
HYPERTROPHIC OSTEOARTHROPATHY
Hypertrophic osteoarthropathy is a combination of generalized periostitis and
digital clubbing.56 In approximately 5% of cases, the condition is inherited and
called primary hypertrophic osteoarthropathy or pachydermoperiostosis. In 95%
of cases, hypertrophic osteoarthropathy is secondary to other disease, often
pulmonary. Bronchogenic carcinoma is the most common cause of secondary
hypertrophic osteoarthropathy, and approximately 5% of cases of bronchogenic
carcinoma have secondary hypertrophic osteoarthropathy. Periostitis, the
hallmark of this condition, is found in multiple sites, usually beginning in the
diaphysis of the long bones and extending toward the metaphysis (Figure 25.22).
Increased vascular perfusion of the affected bones and overgrowth of vascular
connective tissues surrounding the bones, joints, and tendons appear to precede
the periostitis. The clinical presentation is pain and swelling in the affected
extremities. The pathogenesis of secondary hypertrophic osteoarthropathy is
unknown; possibilities described in the literature include a humoral factor, a
neurogenic mechanism, and hypervascularity.
•
FIGURE 25.19 Traumatic brain injury in a patient on long-term antiepileptic drug
therapy (phenytoin) with worsening knee pain after beginning new exercise regimen.
A and B, Coronal T1 and PD FS MRI show incomplete transverse insufficiency
fracture of the medial tibial metaphysis. The fracture site appears to be filled with
unmineralized osteoid (A, arrow), similar to Looser zones in osteomalacia.
•
FIGURE 25.20 Sarcoidosis in the great toe with lacelike appearance.
•
FIGURE 25.21 Sarcoidosis in the fingers with lacelike appearance.
•
FIGURE 25.22 Secondary hypertrophic osteoarthropathy in a patient with lung
cancer. A, Anteroposterior knee radiograph shows thick layer of periosteal bone along
the shaft of the femur and, less visibly, along the shafts of the tibia and fibula. B,
Radionuclide bone scan shows increased cortical activity along the shafts of the lower
extremities.
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Vázquez Díaz M. Multifocal osteonecrosis associated to human immunodeficiency virus infection.
Reumatol Clín. 2012;8(6):361–364.
53. Mehta P, Nelson M, Brand A, Boag F. Avascular necrosis in HIV. Rheumatol Int. 2013;33(1):235–238.
54. Permpalung N, Ungprasert P, Summachiwakij S, Leeaphorn N, Knight EL. Protease inhibitors and
avascular necrosis: a systematic review and meta-analysis. Int J Antimicrob Agents. 2014;44(2):93–95.
55. Neville E, Carstairs LS, James DG. Sarcoidosis of bone. Q J Med. 1977;46(182):215–227
[PMID:866575].
56. Yap FY, Skalski MR, Patel DB, et al. Hypertrophic osteoarthropathy: clinical and imaging features.
RadioGraphics. 2017;37(1):157–195. doi:10.1148/rg.2017160052 [Epub December 9, 2016.
PMID:27935768].
1. Which condition is most closely associated with lacelike bone erosions on

radiographs?
A. Hypervitaminosis A
B. Hypertrophic osteoarthropathy
C. Sarcoidosis
D. Diabetes mellitus
2. The adverse effects of phenytoin therapy on bone are most similar to which of
the following conditions?
A. Osteoporosis
B. Osteopetrosis
C. Osteomyelitis
D. Osteomalacia
3. Tendinosis and tendon rupture are most commonly associated with toxicity
from which class of medication?
A. Bisphosphonates
B. Fluoroquinolones
C. Statins
D. Highly active antiretroviral therapy
4. Which condition is most closely associated with polyostotic periosteal bone

formation in the forearm and lower leg?
A. Hypertrophic osteoarthropathy
B. Hypercortisolism
C. Paget disease
D. Acromegaly

1. C Sarcoidosis is associated with lacelike bone erosions.
2. D Phenytoin is associated with radiologic findings similar to osteomalacia.
3. B Fluoroquinolone toxicity affects the tendons.
4. A Polyostotic periosteal bone formation in the long bones is a feature of
hypertrophic osteoarthropathy.
26
Imaging of Musculoskeletal
Infections
Jennifer L. Favinger and Felix S. Chew
This chapter describes the radiology of musculoskeletal infections.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of musculoskeletal infection, the
4. summarize relevant concepts and knowledge for the following topics: acute and chronic
osteomyelitis, joint infections, spine infections, tuberculosis, fungal infections, cellulitis,
necrotizing soft-tissue infections (NSTI), pyomyositis, gas gangrene, parasitic infestation, Lyme
disease, leprosy, human immunodeficiency virus (HIV) infection and acquired
immunodeficiency syndrome (AIDS), and syphilis.
ACUTE OSTEOMYELITIS
Acute osteomyelitis is a pyogenic infection of the bone that typically occurs in a
child who presents with an acute, systemic febrile illness.1,2 The infection is
usually carried into the bone by the nutrient artery from a preexisting remote site
of infection. Branches of the nutrient artery extend into the metaphysis, where
they loop back and enter large sinusoidal veins. Slowing of blood flow in these
sinusoidal veins permits bacterial colonies to grow and spread into the adjacent
marrow, where small abscesses form. Thrombosis from minor mechanical
trauma may be an associated factor. From the initial focus in the metaphysis, the
acute suppurative inflammatory process may extend throughout the medullary
cavity. Edema and the collection of pus increase the pressure within the closed
space of the medullary cavity, leading to decreased blood flow, thrombosis, and
necrosis. Osteoclasts separate dead bone from living bone. Enzymes elaborated
by inflammatory cells dissolve the necrotic bone. Under pressure, pus exudes
through the cortex into the subperiosteal space by way of haversian and
Volkmann canals. The periosteum becomes elevated by pus, stripping away the
periosteal blood supply and leading to cortical osteonecrosis. Infection may
penetrate the periosteum and extend into the soft tissues (Figures 26.1–26.3).
Where there is capsular investment of the metaphyseal cortex, the joint may
become infected. Reactive periosteal bone forms a shell around the infection,
called the involucrum (Figure 26.4). The central, devitalized bone is called the
sequestrum. Defects in the involucrum, called cloaca, may permit drainage of
pus or extrusion of sequestra through fistulas. Hyperemia causes osteoporosis in
the limb. The common causative organism is Staphylococcus aureus.
Adults at risk for hematogenous osteomyelitis include patients who are
debilitated or immunocompromised, elderly patients with genitourinary tract
infections, patients with peripheral vascular insufficiency (especially diabetes),
and intravenous drug (IVD) users.3,4 Pathogens may also be implanted directly
into the bone during trauma or surgery. Osteomyelitis does not occur in
otherwise healthy adults. An antecedent history of trauma is common, and the
bones of the hands and feet are commonly involved (Figure 26.5). The feet are
particularly vulnerable to infection as a complication of peripheral vascular
disease. In adults, the initial location of infection is epiphyseal and subchondral
because the nutrient artery loops into the sinusoidal veins at the ends of the
bones. The common organism is Staphylococcus, unless the patient is
immunocompromised. In recent years, methicillin-resistant S aureus has also
become a common causative organism. Staphylococcus epidermidis is a
common cause among IVD users. In individuals with sickle cell disease,
Salmonella is another commonly known causative agent. Infections in diabetic
feet tend to be polymicrobial. Contiguous spread of infection may involve the
diaphysis, adjacent soft tissues, and joints. Fistula formation is frequent.
Periosteal reaction may be minimal, especially in the feet. Because the
periosteum is tightly applied, penetration of pus into the soft tissues is common,
but subperiosteal collections are not.
Radiographic changes occur relatively late in acute osteomyelitis. Soft-tissue
swelling with obliteration of fat planes may be seen 3 days after onset, at which
time pus has already penetrated the cortex. Periosteal reaction and osteolysis
may not be evident on radiographs until 5 to 7 days in children and 10 to 14 days
in adults. If the suspected site contains fatty marrow, CT can reveal marrow
infiltration by fluid and pus early in the course of osteomyelitis, before bone
destruction is detectable. CT extends the radiographic ability to define sequestra,
soft-tissue abscesses, sinus tracts, intramedullary and soft-tissue gas, bone
destruction, and reactive bone.
•
FIGURE 26.1 Acute osteomyelitis in the proximal humerus; the patient had a history
of intravenous drug use. A, Radiograph of proximal humerus is normal. B, Coronal T2
FS MRI shows multiple bone abscesses within the proximal humerus.
•
FIGURE 26.2 Osteomyelitis in the femur. Axial T1 FS Gd MRI shows enhancement
in the marrow and surrounding soft tissues, with a layer of periosteal reaction
(involucrum) (arrow).
MRI is highly sensitive and specific in distinguishing between osteomyelitis

and adjacent soft-tissue infection, even in the presence of previous surgery,
fracture, or chronic osteomyelitis. Early marrow edema is evident well before
other imaging studies become abnormal, and subperiosteal or soft-tissue
collections of pus can be identified early. The key finding on MRI is an
abnormal signal within the marrow, low T1 and high T2 signal (Figure 26.6).
Enhancement is generally seen after gadolinium. Abscesses have high T2 signal
with rim enhancement after gadolinium.
The radionuclide bone scan is typically positive within 24 hours of onset, and
a normal bone scan at this time eliminates osteomyelitis as a diagnostic
possibility. Foci of acute osteomyelitis appear as areas of intense activity
because of the hyperemia and reactive osteoblastic activity (Figure 26.7).
Reactive hyperemia and osteoblastic activity are more extensive than the actual
infected area. Devitalized, avascular areas of bone may appear as focal areas of
decreased or absent activity, but the surrounding bone always has increased
tracer uptake. Previous surgery, trauma, and other bone disease may complicate
the interpretation of positive bone scans.
Additional problem-solving imaging tools in suspected osteomyelitis are
nuclear scans with labeled leukocytes or with gallium. Both of these
radiopharmaceuticals localize at sites of aggregation of white blood cells, such
as collections of pus, but both may require delayed imaging, 24 to 72 hours after
injection. The gallium scan may be particularly useful in following the course of
treatment to confirm healing and obviate concern about possible chronic
osteomyelitis (Figure 26.8).
Treatment of bacterial osteomyelitis with systemic antibiotics is effective
when started early. If there are pus formation and bone necrosis, the pus must be
drained and the necrotic bone removed. Acute osteomyelitis may be complicated
by chronic osteomyelitis.
CHRONIC OSTEOMYELITIS
Chronic osteomyelitis may exist many years after acute osteomyelitis, even if the
acute infection was treated appropriately. Systemic antibiotics are ineffective
against organisms sequestered in necrotic bone. Blood cultures are almost
always negative, and cultures of the lesion are often negative as well. A rare
complication of long-standing, chronic, draining osteomyelitis is the
development of malignancy—mostly squamous carcinomas—along the sinus
tract. In chronic osteomyelitis, foci of bacteria persist within bone cavities that
are filled with granulation tissue. Dense bone surrounds the site, and the cortex
may be thickened because of long-term deposition of reactive medullary and
periosteal bone (Figure 26.9). Serpiginous sinus tracts may extend to the skin
surface. Abscesses, sinus tracts, and sequestra may be obscured by the dense
reactive bone, so that CT or MRI may be required. The radionuclide bone scan
shows areas of increased uptake. Scans with gallium or labeled leukocytes
should also be positive. A systematic review and meta-analysis of imaging in
chronic osteomyelitis found that FDG-PET had the highest diagnostic accuracy
for confirming or excluding the diagnosis of chronic osteomyelitis.5
•
FIGURE 26.3 Osteomyelitis in a diabetic patient. A, Radiograph of the foot shortly
after onset shows nonspecific soft-tissue swelling of the third toe. B, Radiograph of
the same foot 6 weeks later shows marked progression of the infection. The soft-
tissue swelling has increased about the third toe, and there are now small collections
of soft-tissue gas. There is osteolysis involving the distal third metatarsal, the proximal
end of the proximal phalanx, and the proximal end of the middle phalanx. The
proximal interphalangeal joint space is grossly widened. The findings are indicative of
osteomyelitis and septic effusion.
•
FIGURE 26.4 Osteomyelitis in the distal fibula. A, Radiograph demonstrating layers
of involucrum (arrow). B, Coronal CT demonstrating the cloaca (white arrow) and
sequestrum (small black arrow). C, Axial CT demonstrating the cloaca (arrow).
•
FIGURE 26.5 Osteomyelitis of the distal phalanx and distal interphalangeal joint of
the third (middle) finger. A, Radiograph demonstrates bony erosion of the distal
phalanx of the middle finger (arrow). B, Radiograph of the third finger following
amputation of the third finger through the middle phalanx.
•
FIGURE 26.6 Osteomyelitis of the right ischial tuberosity in a patient with a sacral
decubitus ulcer tracking down to bone. A, Axial T1 MRI demonstrates characteristic
hypointense signal in the right ischial tuberosity (arrow). B, Axial T2 FS MRI
demonstrates increased signal at the right ischial tuberosity (arrow). C, T1 FS Gd MRI
demonstrates enhancement of the right ischial tuberosity (arrow).
A Brodie abscess is a local, subacute bone abscess that is a fairly common

cause of a solitary bone lesion. Symptoms of recurrent pain and local tenderness
with swelling and erythema may be present for months or years. Most cases
occur in adolescents and young adults, but the reported age range is 6 to
61 years. Men are affected more often than women (by 2:1). The typical location
is the metaphysis or diaphysis of the femur or tibia. A Brodie abscess may begin
de novo, develop in the same site as a preceding episode of acute osteomyelitis,
or follow an acute episode of osteomyelitis at another site. S aureus appears to
be the offending organism.
Radiographically, a Brodie abscess appears as a well-defined lucent area in
cancellous bone with smooth, rounded geographic margins and a thick sclerotic
rind that may merge imperceptibly with the surrounding bone (Figures 26.10 and
26.11). The lesion may appear lobulated with lucent, serpentine tracts extending
along the bone. CT is valuable for defining the reactive sclerosis and can permit
identification of tracts in the bone. The corresponding pathology is an avascular
cavity, typically 1 to 4 cm in size, lined with granulation tissue and filled with
fluid but not frank pus. Thickening of trabeculae adjacent to the lesion by
reactive endosteal bone formation may form the sclerotic rind around the cavity.
Although Brodie abscesses have a characteristic appearance, they may be
confused with other focal bone lesions, including tumors. The key radiologic
feature of a Brodie abscess is the extensive reactive bone formation that has a
sharp interface with the lesion but merges gradually with surrounding normal
bone.
JOINT INFECTIONS
Infections of joints usually follow hematogenous spread of organisms to the
synovium from a preexisting infection in a remote site.6 Less commonly,
adjacent osteomyelitis extends into a joint or a penetrating wound introduces
organisms. The most common infecting organism in adults is S aureus. Gram-
negative bacteria are a common cause of septic arthritis in those with concurrent
genitourinary tract infections, and Streptococcus pneumoniae is a common cause
in those with concurrent lung infections. Other risk factors for septic arthritis
include IVD use, rheumatoid arthritis, systemic lupus erythematosus, total joint
replacement, and advanced age.
•
FIGURE 26.7 Osteomyelitis in a young patient with prior trauma and concern for
infected hardware in the distal tibia. A, Radiograph demonstrates periosteal reaction
along the tibia and marked soft-tissue swelling. B, Tc-99m bone scan of both ankles
demonstrates increased radiotracer uptake on the right.
•
FIGURE 26.8 Resolution of infection. Whole-body gallium scan in a patient with
concern for prior treated osteomyelitis of the left ankle. There is no focal radiotracer
uptake within the left ankle suggesting resolution of infection.
•
FIGURE 26.9 CT of chronic sclerosing osteomyelitis of the clavicle.
From the initial site of inflammation and microabscess formation in the

synovium, the infection may spread to the joint space, bones, and soft tissues.
Proteolytic enzymes released into the joint space by synovial cells and activated
polymorphonuclear leukocytes destroy the ground substance and then the
collagen framework of the articular cartilage. Destruction of the joint takes only
a few days. The usual clinical presentation is the abrupt onset of pain in a
swollen, tender, inflamed joint. The nonspecific physical and laboratory signs of
local and systemic infection may be present, but a preexisting source of infection
is not always obvious. The diagnosis is made by arthrocentesis; injection of
contrast medium under fluoroscopy can confirm intra-articular needle placement
when necessary. The joint fluid is opaque, with a cell count of more than
100 000 WBC/mm3, a differential with more than 85% polymorphonuclear
leukocytes, and a glucose level that is at least 50 mg/dL less than the concurrent
serum level. Cultures of the fluid are almost always positive, and blood cultures
are positive in 50% of cases. On radiographs, acute septic arthritis is evident as
soft-tissue swelling and effusion. Juxta-articular osteoporosis develops, and
within 7 to 10 days, the articular cartilage is gone and the joint space is
narrowed.
•
FIGURE 26.10 Brodie abscess in the distal tibia.
•
FIGURE 26.11 Brodie abscess in the proximal tibia. A, Coronal T1 MRI shows
central lesion with surrounding sclerosis. B, Coronal T1 FS Gd MRI shows
enhancement of the periphery of the lesion but not the center.
Bacterial sacroiliitis is an uncommon spinal infection. In adults the most

common predisposing factors are IVD use and infections of the skin, respiratory
system, and genitourinary tract. In IVD users, the sacroiliac (SI) joint is more
commonly affected by septic arthritis than any other joint (Figures 26.12–26.15).
Prolonged antibiotic treatment and surgical drainage are often required, but the
joint is usually destroyed despite treatment. Secondary degenerative changes
ultimately develop.
Gonococcal arthritis has become rare. Preexisting HIV infection is a risk
factor. Hematogenous dissemination of the sexually transmitted organism causes
fever and arthralgias, typically evident 2 weeks after the initial infection.
Polyarticular and asymmetric involvement is usual, and there is a predilection
for the knees, wrists, and ankles. Arthrocentesis fluid cultures are positive in
fewer than 25%, but the response to antibiotics is rapid, and the outcome is good
in nearly all cases. Radiographs may show only joint effusion and soft-tissue
swelling.
SPINE INFECTIONS
Pyogenic vertebral osteomyelitis occurs in elderly adults with genitourinary tract
infections, patients who are immunocompromised, and IVD users. Organisms
from genitourinary tract infections ascend the vertebral column by way of the
vertebral plexus of Batson, a valveless, venous bed that allows retrograde blood
flow. The initial site of infection is the subcortical bone of the vertebral body
adjacent to the intervertebral disk. The infection typically extends through the
end plate, involving the disk and the adjacent vertebral body. Multiple levels of
involvement can be seen, and the levels may be contiguous or noncontiguous.
Lateral extension results in paraspinal abscess; posterior extension can result in
epidural abscess, cord compression, and meningitis.
The radiographic finding is disk space narrowing with destruction of the
facing vertebral end plates. As the process evolves, increasing reactive bone
production and sclerosis occur in the affected vertebral bodies on both sides of
the involved disk space, often making it appear widened. Bony ankylosis is one
eventual outcome of this process. Paravertebral soft-tissue swelling may indicate
extension into the soft tissues. CT and MRI can delineate the anatomic extent of
involvement (Figure 26.16).7
•
FIGURE 26.12 Septic arthritis. A, Hip radiograph 1 month after onset shows diffuse
cartilage loss. B, Three untreated months after onset, the femoral head and
acetabulum have been destroyed. β-Hemolytic Streptococcus was cultured from the
hip when it was surgically drained and debrided. C, Two months after surgery, the
bone has healed, but the femoral head and neck were sacrificed.
•
FIGURE 26.13 Septic arthritis in a 22-year-old man with streptococcal bacteremia,
necrotizing soft-tissue infection, and limited range of shoulder motion. There was a
history of intravenous drug abuse. A, Grashey radiograph of left shoulder shows loss
of glenohumeral cartilage space and possible erosion superiorly . B, Follow-up CT
5 months later shows marked diffuse glenohumeral cartilage loss, subchondral bone
erosion, and osteopenia.
The clinical presentation is fever, back pain, and stiffness. Diagnosis is often
delayed; radiographic findings may not be apparent until 2 to 8 weeks after
onset. In 60% of cases, the recovered organism is S aureus; in 30% of cases, the
organisms are species of Enterobacteriaceae. In 40% of cases, a remote source of
infection is known (usually genitourinary tract, skin, or respiratory tract).
TUBERCULOSIS
Tuberculosis is becoming more common in North America but is usually
associated with immunocompromised patients or immigrant populations.
Musculoskeletal disease occurs because of hematogenous spread, typically from
the lungs. Approximately half of all cases of musculoskeletal tuberculosis affect
the spine, also known as Pott disease or tuberculous spondylitis. The infection is
often insidious with mild symptoms, which can result in a delay in diagnosis.
The thoracolumbar junction is the most commonly affected site, but involvement
of the cervical and thoracic region, posterior elements, and SI joints is known to
occur. Involvement of multiple contiguous levels is frequent, but a hallmark of
tuberculous infection of the spine is sparing of or very late involvement of the
intervertebral disk (Figure 26.17). The infection usually begins in the anterior or
anterolateral aspect of the vertebral body at an end plate. Infection may spread
by extending into the disk space, along the subligamentous space, or into the
paraspinal soft tissues. Paravertebral psoas abscesses may burrow into the groin
or thigh. Tuberculous spondylitis is also one of the known causes of vertebra
plana or pancake vertebra (Figure 26.18).
FIGURE 26.14 • Septic arthritis following cat bite injury. There are marked
asymmetric soft-tissue swelling of the index finger and diffuse chondrolysis of the
proximal interphalangeal joint. There is juxta-articular osteoporosis. A to C, Lateral,
oblique, and posteroanterior radiographs.
•
FIGURE 26.15 Septic sacroiliitis in an intravenous drug user. Coronal T2 FS MRI
shows bony erosions, subchondral edema, and fluid collection involving both
sacroiliac joints (arrow).
Tuberculous osteomyelitis may result from contiguous spread from an

adjacent joint or from hematogenous spread.8 The ends of long bones are
typically involved, and there may be multiple sites of involvement within the
same bone or dispersed throughout the skeleton. On radiographs, osteolysis,
erosions, and osteoporosis are the dominant features. Soft-tissue extension with
burrowing abscesses may be present, but reactive bone formation is sparse or
absent. On MRI, the region of involvement has low T1 and high T2 signal, with
enhancement after gadolinium. Periosteal reactive bone and subperiosteal
involvement tend to be absent, unlike acute pyogenic osteomyelitis (Figure
26.19).
Tuberculosis may spread to the joints, resulting in a granulomatous synovial
infection that requires synovial biopsy or joint aspiration for diagnosis. In the
usual situation, the process is monarticular, and there is osteomyelitis adjacent to
the involved joint. The classic radiographic appearance is juxta-articular
osteoporosis, peripherally located erosions, and gradual joint space narrowing
(Figure 26.20). However, multifocal disease, periostitis, sclerosis, and large soft-
tissue abscesses may occur. Few cases of tuberculous tenosynovitis have been
reported, with fluid accumulation within the tendon sheath and tenosynovial
thickening (Figure 26.21). Symptoms are often vague, including erythema, pain,
and limitation of joint movement, which can result in delay in diagnosis. As with
other chronic forms of tuberculosis infection, ESR and CRP levels will be
elevated.
•
FIGURE 26.16 Vertebral discitis and osteomyelitis at L2-L3 with destruction of the
adjacent end plates. A, Sagittal CT shows erosion at the adjacent end plates
(arrowheads). B, Sagittal STIR MRI shows edema in the L2 and L3 vertebral bodies.
C, Axial T1 FS Gd MRI at L3 shows surrounding soft-tissue enhancement. D, Sagittal
T1 FS Gd MRI shows enhancement of the L2 and L3 vertebral bodies.
•
FIGURE 26.17 Tuberculous spondylitis. Sagittal T1 FS Gd MRI demonstrates
enhancement and destruction of multiple midthoracic vertebral bodies, without
enhancement of the intervening disks.
FUNGAL INFECTIONS
Fungal infections are caused by dimorphic pathogenetic organisms. The mycelial
form of the organism produces infectious spores that may be inhaled and
converted to yeastlike pathogens in the host. The entire range of fungal
infections that occurs in the lungs may also involve the musculoskeletal system,
especially coccidioidomycosis, histoplasmosis, and blastomycosis. The
infections are often low grade and chronic but may become virulent when host
defenses are compromised. Opportunistic infections such as candidiasis may also
occur in immunocompromised individuals. Radiologic features of fungal
osteomyelitis include osteolysis with discrete or permeated margins, surrounding
sclerosis that is less florid than in bacterial infections, and variable amounts of
periosteal reaction (Figure 26.22). Extensive bone sclerosis and formation of
sequestra are unusual. Fungal septic arthritis has a nonspecific appearance with
soft-tissue swelling, diffuse joint space loss, and central and marginal erosions of
bone. The progression of disease is slower, and the host bone reaction is milder
than pyogenic infections.
•
FIGURE 26.18 Vertebra plana in tuberculous spondylitis. A, Sagittal T2 FS MRI and
B, sagittal T1 FS Gd MRI demonstrate complete collapse of the T11 vertebral body
(arrows) with edema and enhancement in the adjacent T10 and T12 vertebral bodies
and the surrounding soft tissues. There is significant mass effect on the spinal cord.
•
FIGURE 26.19 Tuberculosis osteomyelitis. A, Coronal CT of the knee shows focal
lucency (arrow) with sclerotic center at the medial tibial metaphysis with overlying
soft-tissue swelling. There is no reactive bone formation. B, Coronal T1 MRI shows
focal bone lesion with sequestrum, cortical penetration, and soft-tissue swelling. C,
Coronal T2 FS MRI shows high signal within the lesion and adjacent soft tissues.
There is a joint effusion.
FIGURE 26.20 • Tuberculous arthritis. A and B, Posteroanterior and lateral
radiographs of the thumb show destruction of the metacarpophalangeal joint with
osteoporosis and minimal reactive bone formation.
CELLULITIS AND SUBCUTANEOUS ABSCESS

Cellulitis is diffuse purulent inflammation of the loose subcutaneous soft
tissues.9 The process may disseminate along anatomic planes. On radiographs,
cellulitis is evident as soft-tissue swelling and obliteration of normal tissue
planes, the same early radiographic features of osteomyelitis. If a gas-forming
organism is involved, soft-tissue gas may be present. The 3-phase bone scan can
distinguish between cellulitis and osteomyelitis. On immediate postinjection
flow images (radionuclide angiogram) and on blood pool images (obtained
5 minutes after injection, reflecting distribution of radionuclide in the vascular
space), both cellulitis and osteomyelitis show diffusely increased soft-tissue
uptake. However, on delayed images (obtained 2 hours after injection), cellulitis
shows no focal abnormality, but osteomyelitis shows focal tracer uptake in bone
at the site of infection. MRI and CT are also highly accurate in delineating soft-
tissue infections. On MRI, cellulitis is evident as reticular subcutaneous edema
and enhancement after gadolinium injection (Figure 26.23). Edema and
enhancement of the underlying fascia, muscle, or bone are indicative of fasciitis,
myositis, and osteomyelitis, respectively. If present, soft-tissue abscesses show
rim enhancement after gadolinium injection. Soft-tissue gas is more difficult to
identify on MRI than on CT.
Noninfectious subcutaneous edema—as might occur after a bite from a spider
or snake or after an allergic reaction to a bee sting—results in soft-tissue edema.
The radiologic appearance is similar to infectious cellulitis except gas formation
and abscess formation do not occur. Osteomyelitis of the underlying bone does
not occur.
•
FIGURE 26.21 Tuberculous tenosynovitis. A and B, Sagittal and axial T1 FS Gd
MRI demonstrate enhancing fluid collections within the flexor tendon sheaths of the
ankle in a young patient with chronic tuberculous infection.
•
FIGURE 26.22 Candidal osteomyelitis of the humerus. CT shows focal bone
destruction and minimal reactive change.
Cellulitis and skin infections may organize into abscesses in the subcutaneous
compartment. Superficial abscesses may be apparent on physical examination,
but imaging may be required to identify deeper abscesses. Sonography, CT with
contrast, and MRI without and with gadolinium would be the examinations of
choice. If NSTI is suspected, CT is better for demonstrating soft-tissue gas. MRI
is better for demonstrating osteomyelitis. Sonography can demonstrate or
exclude subcutaneous abscesses and provide guidance for percutaneous
aspiration (Figure 26.24).
PYOMYOSITIS
Pyomyositis is caused by S aureus in approximately 90% of cases; most of the
remaining cases are caused by Streptococcus. Because healthy muscle is
resistant to hematogenous infections, pyomyositis usually is found in the
presence of predisposing conditions such as local trauma, nutritional deficiency,
immunocompromise, or concurrent infections elsewhere.10 Pyomyositis is
characterized by a bacterial abscess within skeletal muscle and used to be
considered a tropical disease (hence it was previously called tropical
pyomyositis or myositis tropicans) but is also found in temperate climates,
particularly in patients with immunocompromise, HIV, and IVD use. Imaging by
sonography, CT, or MRI shows extensive inflammation and abscess formation
(Figures 26.25 and 26.26). Direct extension to bone may occur. The definitive
diagnosis is made by aspiration and culture. Infectious myositis can also occur
beyond bacterial infections. Risk factors also include rhabdomyolysis, overlying
cellulitis, insect bites, and injection of illicit drugs. Depending on the size and
location of the abscess, compartment syndrome is a potential complication.
NECROTIZING SOFT-TISSUE INFECTION

NSTI, also known as necrotizing fasciitis, is an uncommon, deep soft-tissue
infection caused by group A streptococci.11,12 Known in the lay literature as the
disease caused by “flesh-eating bacteria,” NSTI has a mortality rate of
approximately 25%. It is previously called necrotizing fasciitis, but now more
commonly called necrotizing soft-tissue infection, given the involvement of
muscle and other deep soft-tissues in addition to the fascia itself. Although it
occurs more frequently in diabetics, IVD users, immunosuppressed patients, and
patients at risk for other infections, it may also occur in young and previously
healthy patients, including athletes. The abdominal wall, extremities, and
perineum are the most common sites of involvement, and NSTI may occur with
streptococcal toxic shock syndrome. Both direct implantation of bacteria through
a break in the skin and hematogenous spread may occur. Patients present with
severe local pain, characteristically described as pain out of proportion to
examine, skin changes, and systemic toxicity. Radiographs of NSTI in the
extremities may show extensive subcutaneous edema and gas (Figures 26.27 and
26.28). The gas may track along fascial planes. On CT, gas in the soft tissues is
more easily identified than on radiographs (Figure 26.29). It is important to note
that the absence of soft-tissue gas does not exclude the infection, particularly on
radiographs where soft-tissue gas can be difficult to identify. Diffuse thickening
of the skin, edema of the subcutaneous tissues, thickening of the fascia, and fluid
collections are other features of CT. On MRI, involved fascial planes have low
T1 and high T2 signal. Enhancement of the fascia after gadolinium is indicative
of inflammation, whereas lack of enhancement is indicative of tissue necrosis.
•
FIGURE 26.23 Cellulitis of the foot in a diabetic patient. A, Axial T1 MRI shows low
signal in the lateral subcutaneous tissues (arrow). B, Axial STIR MRI shows edema
(arrow). C, Axial T1 FS Gd MRI shows enhancement (arrow).
•
FIGURE 26.24 Subcutaneous abscess in posterior arm. A, Transverse sonogram of
the posterior arm shows a complex fluid collection in the subcutaneous compartment.
B, Percutaneous aspiration of the collection was performed under ultrasound
guidance. Static image from the procedure shows the needle in place.
•
FIGURE 26.25 Pyomyositis with an abscess in the distal sartorius muscle in a
patient following a femoral to popliteal bypass graft surgery. Axial contrast-enhanced
CT demonstrates the rim-enhancing intramuscular abscess (arrow) with surrounding
soft-tissue edema.
GAS GANGRENE
Clostridial contamination of traumatic wounds may produce extensive tissue
damage and gas formation in devitalized tissues (gas gangrene).13 The causative
agent, Clostridium perfringens, is widely distributed in nature. Unlike deep
group A streptococcal infections, clostridial infections spare the fascia but cause
rapid necrosis of muscle. Clostridial myositis is an acute, rapidly progressive,
invasive infection of muscle that often results in myonecrosis and systemic
toxicity. Exotoxins elaborated by the bacteria promote the rapid spread of
infection by destroying healthy tissue and interfering with normal host
responses. Clostridial myonecrosis has a classic radiographic appearance of
extensive featherlike linear collections of gas that are widely dispersed
throughout the affected muscles (Figure 26.30). Therapy for clostridial
myonecrosis includes surgery, antibiotics, and hyperbaric oxygen, with reported
mortality rates of 5% to nearly 30%.
FIGURE 26.26 • Pyomyositis with abscess in the soleus muscle of an

immunosuppressed patient. A, Axial T2 MRI shows heterogeneous high signal in a
lesion (white arrow) in the soleus, with extensive subcutaneous edema and
obliteration of the normal fat between the muscle fascicles. B, Axial T1 FS Gd MRI
shows enhancement of the superficial posterior compartment and the rim of the
abscess (black arrow).
•
FIGURE 26.27 Necrotizing fasciitis of upper right arm in a patient with acute
promyelocytic leukemia, showing gas (arrow) in the subcutaneous tissues and
muscles.
PARASITIC INFESTATION
Cysticercosis—infestation by the larval form of the pork tapeworm—may cause
dense, widespread calcifications in the muscular tissues. Calcification is a late
finding that is seen years after infestation. Larval death evokes a foreign body
reaction that causes localized tissue necrosis with caseation. The calcifications
may be up to 3 cm in size and tend to be oriented with the muscle fibers (Figure
26.31). Parasitic infestation with other worms is unusual in the United States
except among immigrants from endemic tropical regions of the world.
•
FIGURE 26.28 Necrotizing soft-tissue infection in the foot in a patient with diabetes.
Lateral radiograph demonstrates extensive soft-tissue gas within the dorsum of the
foot. Amputation was necessary.
LYME DISEASE
Lyme disease is an inflammatory multisystem disease that follows infection by
the spirochete Borrelia burgdorferi. The vector is the deer tick, an insect
endemic to forested areas of the United States, Europe, and Australia. Clinical
findings in the acute infection include a rash and flulike syndrome. Months later,
multisystem involvement may become apparent. In the musculoskeletal system,
arthralgias of sudden onset and short duration appear, sometimes migratory and
recurrent. One or more joints may be involved, most frequently the large joints
and also the temporomandibular joints, SI joints, and joints of the hands and feet.
The radiographic appearance is nonspecific and may include joint effusion,
juxta-articular osteoporosis, subchondral marrow edema, bone erosions,
enthesopathy, and periostitis.14 Occasionally, a chronic inflammatory
oligoarthritis that resembles rheumatoid arthritis develops, particularly in the
knees.
•
FIGURE 26.29 Necrotizing soft-tissue infection in the left shoulder in a patient with
intravenous drug use. Contrast-enhanced CT demonstrates subcutaneous, deep
fascial and intramuscular edema. Additionally, there are numerous fluid collections
and bubbles of gas in the soft tissues.
•
FIGURE 26.30 Clostridial myonecrosis in the lower leg with widespread dissection
of gas along muscle fibers, resulting in a feathery appearance.
•
FIGURE 26.31 Cysticercosis with calcified larvae in the musculature throughout the
lower leg in a trauma patient.
LEPROSY
Leprosy is a chronic granulomatous infection of the skin, peripheral nerves,
mucous membranes, and other organs. It becomes evident after a lengthy
incubation. Caused by Mycobacterium leprae, the disease is virtually unknown
in the United States except among immigrants from Africa, South America, and
parts of Asia. The most common radiographic abnormalities in leprosy are
related to involvement of the peripheral nerves. Atrophic neuropathic
osteoarthropathy may result from denervation and repetitive minor injury. On
radiographs, findings may include atrophy, resorption, and tapering of the ends
of the bones, particularly of the digits of the hands and feet (Figure 26.32).
Involvement is generally asymmetric. Leprous periostitis, osteitis, and
osteomyelitis occur, but they do so infrequently. There is a propensity for the
development of squamous cell carcinoma at sites of cutaneous ulcerations. There
is an increased risk of developing lymphoma and leukemia.
HIV INFECTION AND AIDS

Infection with HIV devastates cellular-mediated immunity, leading at a variable
rate to AIDS and death. Musculoskeletal manifestations are less common than
manifestations in the central nervous system, the gastrointestinal tract, and the
lungs. These include infections, neoplasms, and rheumatologic conditions.15
Osteomyelitis may be caused by common and opportunistic organisms,
including S aureus, Salmonella, tuberculosis, fungus, and Rochalimaea henselae
(the rickettsial species that causes bacillary angiomatosis).16 Bacterial myositis
and septic arthritis may also be caused by common and opportunistic organisms.
Non-Hodgkin lymphoma has an incidence 60 times greater in patients with
AIDS than in the general population. Primary and secondary involvement of the
marrow is common. Kaposi sarcoma also may metastasize to bone. Anemia is
common in HIV-positive patients and leads to reconversion of fatty (yellow)
marrow to hematopoietic (red) marrow. Polymyositis and inflammatory arthritis
have been reported in patients with AIDS. HIV is also a known risk factor for
avascular necrosis.
FIGURE 26.32 • Leprosy. Foot radiograph of a patient with known leprosy
demonstrates acroosteolysis and thin proximal phalanges.
SYPHILIS
Syphilis is a sexually transmitted infection caused by the spirochete Treponema
pallidum. It can be congenital or acquired. If left untreated, the infection can
progress through stages to affect the musculoskeletal system. Arthralgias are one
of the hallmarks of secondary syphilis. Tertiary syphilis can affect the
musculoskeletal system and lead to progressively destructive arthritis. This can
be due to direct infection, known as gummatous arthritis, due to granulomatous
infection of a joint, or due to tabetic arthropathy or Charcot joint, which is
neuropathic in origin. This neuroarthropathy eventually results in painless
destruction and disorganization of a joint and the surrounding structures. These
conditions are rarely if ever seen in our experience.
References
1. Whyte NS, Bielski RJ. Acute hematogenous osteomyelitis in children. Pediatr Ann. 2016;45(6):e204–
e208. doi:10.3928/00904481-20160428-01 [PMID:27294494].
2. Peltola H, Pääkkönen M. Acute osteomyelitis in children. N Engl J Med. 2014;370(4):352–360.
doi:10.1056/NEJMra1213956 [PMID:24450893].
3. Lew DP, Waldvogel FA. Osteomyelitis. Lancet. 2004;364(9431):369–379 [PMID:15276398].
4. Tehranzadeh J, Wong E, Wang F, et al. Imaging of osteomyelitis in the mature skeleton. Radiol Clin
North Am. 2001;39:223–250.
5. Termaat MF, Raijmakers PG, Scholten HJ, Bakker FC, Patka P, Haarman HJ. The accuracy of
diagnostic imaging for the assessment of chronic osteomyelitis: a systematic review and meta-analysis.
J Bone Joint Surg Am. 2005;87(11):2464–2471 [PMID:16264122].
6. Dubost JJ, Soubrier M, Sauvezie B. Pyogenic arthritis in adults. Joint Bone Spine. 2000;67(1):11–21
[PMID:10773964].
7. Stäbler A, Reiser MF. Imaging of spinal infection. Radiol Clin North Am. 2001;39(1):115–135
[PMID:11221503].
8. Soler R, Rodríguez E, Remuiñán C, Santos M. MRI of musculoskeletal extraspinal tuberculosis. J
Comput Assist Tomogr. 2001;25(2):177–183 [PMID:11242210].
9. Hirschmann JV, Raugi GJ. Lower limb cellulitis and its mimics: part I. Lower limb cellulitis. J Am Acad
Dermatol. 2012;67(2):163.e1–e12; quiz 175-6. doi: 10.1016/j.jaad.2012.03.024 [PMID: 22794815].
10. Theodorou SJ, Theodorou DJ, Resnick D. MR imaging findings of pyogenic bacterial myositis
(pyomyositis) in patients with local muscle trauma: illustrative cases. Emerg Radiol. 2007;14(2):89–96
[Epub February 28, 2007. PMID:17333082].
11. Fontes Jr RA, Ogilvie CM, Miclau T. Necrotizing soft-tissue infections. J Am Acad Orthop Surg.
2000;8:151–158.
12. Wong CH, Chang HC, Pasupathy S, Khin LW, Tan JL, Low CO. Necrotizing fasciitis: clinical
presentation, microbiology, and determinants of mortality. J Bone Joint Surg Am. 2003;85:1454–1460.
13. Patzakis MJ. Clostridial myonecrosis. Instr Course Lect. 1990;39:491–493 [PMID:2186141].
14. Lawson JP, Steere AC. Lyme arthritis: radiologic findings. Radiology. 1985;154(1):37–43
[PMID:3964949].
15. Steinbach LS, Tehranzadeh J, Fleckenstein JL, et al. Human immunodeficiency virus infection:
musculoskeletal manifestations. Radiology. 1993;186:833–838.
16. Hirsch R, Miller SM, Kazi S, et al. Human immunodeficiency virus-associated atypical mycobacterial
skeletal infections. Semin Arthritis Rheum. 1996;25:347–356.
1. What is the most common route of bone infection in the diabetic foot?
A. Contiguous spread from ulcers
B. Septic emboli
C. Lymphangitic spread
D. Penetrating trauma
2. What is the typical appearance of acute osteomyelitis on MRI?
A. High bone marrow signal on T1 MRI
B. Low bone marrow signal on T2 FS MRI
C. High bone marrow signal on T1 FS Gd MRI
D. Low bone marrow signal on GRE MRI
3. Gas in the soft tissues detected on CT is most suggestive of which condition?

A. Parasitic infestation
B. Tuberculosis
C. Acute osteomyelitis
D. Necrotizing soft-tissue infection
4. Which radiographic finding is most common in chronic osteomyelitis?

A. Pathologic fracture
B. Sclerosis
C. Layered periosteal reaction
D. Soft-tissue calcification

1. A Foot ulcers are the common source of foot osteomyelitis.
2. C The typical appearance of acute osteomyelitis on MRI is high T2 signal,
low T1 signal, and enhancement.
3. D Soft-tissue gas may be present with necrotizing soft-tissue infection.
4. B Sclerosis is a characteristic radiographic feature of chronic osteomyelitis.
27
Imaging of Bone Marrow Conditions
Erika M. Nealey, Blake Carlson, and Felix S. Chew
This chapter describes the imaging of various nonneoplastic bone marrow

conditions.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of the imaging of bone marrow disorders, the
4. summarize relevant concepts and knowledge for the following topics: osteonecrosis of the
femoral head, subchondral insufficiency fracture of the knee, Kienbock disease, marrow infarct,
bone marrow edema syndrome, sickle cell disease, thalassemia, hemophilia, myelofibrosis,
and Gaucher disease.
BONE MARROW
The bone marrow is one of the largest organs of the body. Confined to the
intramedullary space of bone, it consists of a meshwork of trabecular bone with
fat cells, myeloid cells, reticulum cells, and supporting structures. At birth, the
marrow cavities of tubular bones, flat bones, and vertebrae have a predominance
of hematopoietic cells. With advancing age, the hematopoietic (red) marrow
regresses and is replaced by fatty (yellow) marrow, beginning distally in the
extremities and progressing to encompass incompletely the pelvis, spine, and
cranium by the end of childhood (Figure 27.1). The process may reverse
(marrow reconversion) when there is an increased demand for hematopoiesis, as
may occur in anemia or replacement of normal hematopoietic marrow by a
pathologic process (Figure 27.2). Any part of the skeleton that ossifies after the
regression of red marrow, such as the epiphyses in the extremities, will have
yellow marrow to start with and cannot reconvert to red marrow.
Radiographic findings of marrow disorders are indirect and nonspecific.
When chronic marrow space expansion occurs in the growing skeleton, adaptive
bone changes may occur during the development of the bone. Actual
enlargement of the marrow space alters the normal bony contours; such changes
do not occur acutely nor do they occur in the adult. The best method for direct
imaging of the bone marrow is MRI. Because marrow is a conglomeration of
different tissues, the appearance on MRI may vary with the composition of the
marrow as well as with the particular technical parameters.1 In general, yellow
marrow has the predominant signal characteristics of fat and red marrow has
signal characteristics more similar to muscle. Nuclear scans with technetium-
99m (99mTc) sulfur colloid or 99mTc-methylene diphosphonate can provide
physiologic assessments of the reticuloendothelial marrow elements and the
surrounding bone, respectively.
OSTEONECROSIS
Most bones have a dual blood supply. The periosteum has a rich network of
vessels that supplies the periosteal portion of the cortex. The endosteal blood
supply enters through one or more nutrient arteries and supplies the marrow, the
trabecular bone, and the endosteal portion of the cortex. Portions of bone that are
covered with articular cartilage or enclosed within joint capsules have no
periosteum and therefore have only an endosteal blood supply, leaving them
more vulnerable to ischemic infarction.
Femoral Head
The femoral head is the most important clinical site of osteonecrosis.2 Men are
affected more often than women (4:1), and the usual age range of patients is 30
to 70 years. The typical presentation is abrupt onset of hip pain without trauma.
In 50% of cases, bilateral involvement is present; bilateral disease is usually
asymmetric. The predominant blood supply to the femoral head is through lateral
epiphyseal vessels that enter posterosuperiorly. Only a small portion of the head
is supplied through vessels in the ligamentum teres.
Osteonecrosis begins with interruption of the blood supply to the femoral
head. The precise event that initiates the loss of circulation is unknown, although
there are a large number of associated conditions, including alcoholism and
systemic corticosteroids (Table 27.1). One possible event is an increase in
intraosseous pressure within the femoral head; when this pressure exceeds the
perfusion pressure, blood flow stops. Ischemic necrosis of the marrow and bone
follows with the onset of pain, but radiographs are normal. Intramedullary
pressure measurements of the proximal femur are elevated. The typical
distribution of infarction is a wedge-shaped region under the weight-bearing
surface of the femoral head. The articular cartilage itself remains viable because
its nutrition is derived from the synovial fluid. After infarction, the avascular
area becomes revascularized from the periphery, and creeping substitution of
devitalized bone occurs. When repair begins, radiographs may show an increase
in bony density around the periphery of the infarction. This increased peripheral
density may slowly progress centrally as repair proceeds (Figure 27.3).
Sometimes, the dead bone is incompletely resorbed, and a sclerotic zone remains
indefinitely (Figure 27.4). Because this repair process involves both resorption
and replacement of bone, the mechanical strength may decrease transiently and
subchondral insufficiency fractures may result. Insufficiency fractures of the
subchondral bone may be recognized by a crescentic lucent zone that separates
the fragment, a radiographic feature called the crescent sign (Figure 27.5).
Insufficiency fractures lead to segmental collapse of the femoral head, resulting
in deformity and secondary osteoarthrosis of the hip (Figure 27.6).
•
FIGURE 27.1 Normal yellow (fatty) bone marrow at the knee. A, Coronal T1 MRI
shows fatty marrow filling the distal femur and proximal tibia. The signal is similar to
that of subcutaneous fat. B, Coronal PD FS MRI shows equal fat suppression of the
marrow signal and the subcutaneous fat.
•
FIGURE 27.2 Red marrow reconversion at the knee. A, Coronal T1 MRI shows less
bright signal in the metaphyses and shafts of the distal femur and proximal tibia,
corresponding to regions of reconversion of yellow marrow to red marrow. B, PD FS
MRI shows slightly increased signal in the regions of red marrow reconversion, similar
to muscle but much less than fluid. Note that there is no red marrow in the epiphyses.
MRI is the most accurate modality for detecting femoral head osteonecrosis,
with sensitivities and specificities of 100% reported in multiple studies (Figure
27.7).3 The region of osteonecrosis is evident as a loss of the normal bright
marrow T1 signal on MRI. Characteristically, the region of involvement is the
superior weight-bearing quadrant of the femoral head. If marrow edema is
present in the femoral head and sometimes femoral neck, then the osteonecrosis
is thought to be acute or subacute. Hip effusion is commonly present. As the
osteonecrosis begins to remodel, edema and revascularization results in the
double line sign. On T2 FS MRI, the region of osteonecrosis is circumscribed by
a peripheral zone of high signal and an adjacent outer zone of low signal (Figure
27.8). MRI can also depict late osteonecrosis and subchondral collapse of the
femoral head (Figure 27.9). The radionuclide bone scan may initially show loss
of radionuclide accumulation in the avascular stage with subsequent variable
increases in accumulation in the reparative stage. The nuclear scan is less
sensitive than MRI and gives poor anatomic detail. The common asymmetric
bilaterality of osteonecrosis of the femoral head may complicate interpretation of
the bone scan. The most sensitive test for early osteonecrosis of the femoral head
is intramedullary pressure measurement.
Table 27.1 CLINICAL CONDITIONS ASSOCIATED WITH OSTEONECROSIS OF THE

FEMORAL HEAD IN ADULTS
Unilateral Bilateral
Commonly Associated Conditions
Idiopathic Alcoholism
Trauma Corticosteroids
Surgery Idiopathic
Uncommonly Associated Conditions
Gout Arteriosclerosis
Hemophilia Caisson disease
Infection Coagulopathy
Cushing disease
Gaucher disease
Hemoglobinopathy (Sickle cell disease)
HIV/retroviral therapy
Hyperlipidemia
Pancreatitis
Pheochromocytoma
Systemic lupus erythematosus
•
FIGURE 27.3 Osteonecrosis of the femoral head. Anteroposterior radiograph of the
hip showing subtle femoral head sclerosis (arrow).
•
FIGURE 27.4 Osteonecrosis. Radiograph of the left femoral head shows sclerosis.
Precollapse osteonecrosis may be treated by decompression of the femoral

head, usually by drilling a hole in the lateral cortex through the neck and into the
head. Concurrent implantation of autologous bone marrow aspirate containing
high concentrations of mesenchymal stem cells may also be performed.
Sometimes a tantalum insert or vascularized bone graft may be placed to
encourage bone growth. Bisphosphonates have also been advocated for
treatment of precollapse osteonecrosis. These and other therapies remain
controversial. Once subchondral collapse has begun, the natural history
ultimately leads to end-stage osteoarthrosis, and replacement arthroplasty
becomes the remaining treatment option.
Subchondral Insufficiency Fracture of the Knee

The entity formerly called spontaneous osteonecrosis of the knee is now known
as subchondral insufficiency fracture of the knee. It is now theorized that the
process begins as a subchondral insufficiency fracture and then in some patients
may progress to osteonecrosis and subchondral collapse. The typical patient
population is adult women older than 50 years; obesity and osteoporosis are also
risk factors. The medial femoral condyle is most commonly involved, but the
lateral femoral condyle or even the tibial plateau may be affected. If no
osteonecrosis occurs, the condition may be self-limited and resolve within a few
months; if osteonecrosis occurs, subchondral collapse and rapid progressive
secondary osteoarthritis will ensue. Radiographs may be normal in early stages
of the disease; sclerosis, subchondral lucency, flattening of the condyle, and
eventual secondary degenerative joint disease may be subsequently seen. On
MRI, there is a T1 and T2 hypointense subchondral line denoting the
insufficiency fracture; there is characteristic extensive flame-shaped associated
marrow edema in the affected condyle4 (Figure 27.10). As the area becomes
revascularized and remodels, the region of osteonecrosis becomes better defined
by low signal around the periphery. If the lesion progresses to subchondral
collapse, the condyle may become flattened and overlying articular cartilage
may be lost.
•
FIGURE 27.5 Osteonecrosis with crescent sign. A, Anteroposterior radiograph
shows subtle femoral head sclerosis. B, Frog lateral radiograph shows crescent-
shaped lucency (arrow) separating the subchondral cortex of the femoral head.
•
FIGURE 27.6 Osteonecrosis with subchondral collapse. A and B, Anteroposterior
radiographs of both hips show bilateral femoral head osteonecrosis with subchondral
collapse.
Kienbock Disease
Kienbock disease is defined as avascular necrosis of the lunate. The highest
incidence of Kienbock disease is in males in the third through fifth decades of
life. Although the precise etiology of Kienbock disease remains uncertain, there
is an association with negative ulnar variance; as such, various authors have
postulated that the disease is related to pathologic force loading on the lunate.5
As in other types of osteonecrosis, MRI is most sensitive for early detection,
with marrow edema being the first manifestation. Sclerosis and subchondral
collapse become evident by radiography as the disease progresses (Figure
27.11). End-stage Kienbock disease is characterized by carpal instability, with
widening of the scapholunate interval, rotatory subluxation of the scaphoid, and
ultimately development of radiocarpal osteoarthritis (Figure 27.12). Early stage
Kienbock disease may be treated by immobilization; if immobilization is
ineffective, radial shortening osteotomy or other surgical correction of force
loading may be performed, with or without vascularized bone grafting6 (Figure
27.13). Advanced Kienbock disease is treated with proximal row carpectomy
and proximal interosseous neurectomy for symptomatic relief.
•
FIGURE 27.7 Osteonecrosis with marrow edema. A, Coronal T2 FS MRI shows
extensive marrow edema in the femoral head and neck. B, Coronal T1 MRI shows
fatty marrow in the infarcted sector of the head (arrow) and low signal in the
surrounding region.
•
FIGURE 27.8 A, Axial T2 FS MRI shows double line sign of femoral head avascular
necrosis with adjacent peripheral zones of high and low signal (arrow). B, Coronal T1
MRI shows serpentine margin of the infarction.
Osteonecrosis of Other Sites

Osteonecrosis has been described at various sites in the skeleton. The
pathophysiology is the same regardless of site and follows the stages described
earlier: ischemia, revascularization, repair, deformity, and osteoarthrosis.
Examples include osteonecrosis of the humeral head (Figure 27.14),
osteonecrosis of the jaw, and medullary infarcts within the long bones. On MRI,
remodeling medullary infarcts are usually multiple and have a diagnostic
appearance. They have an irregular, serpiginous, sharply defined low signal
border on T1 and PD images (Figures 27.15 and 27.16). If there is a surrounding
zone of high T2 signal, then the infarcts are acute or subacute. This zone of high
T2 signal corresponds to the margin of revascularization and remodeling.
Contemporaneous radiographs are often normal, but the infarcted marrow may
eventually calcify (Figure 27.17). This dystrophic calcification in infarcts may
resemble the mineralized matrix of an endosteal cartilage tumor.
•
FIGURE 27.9 Osteonecrosis with subchondral fracture (different patients). A,
Sagittal PD FS MRI showing avascular necrosis with subchondral insufficiency
fracture (arrow) and associated edema. B, Coronal T1 MRI of late stage avascular
necrosis with femoral head collapse (arrow) .
•
FIGURE 27.10 A and B, Coronal PD FS and T1 MRI showing T1 and T2
hypointense subchondral fracture line (arrow) and flame-shaped marrow edema
(short arrows) characteristic of subchondral insufficiency fracture of the knee.
Osteonecrosis is a common complication of skeletal trauma. Bone fragments

with a single endosteal blood supply are highly vulnerable to its disruption by
fracture displacement, including the proximal pole of the scaphoid, the radial
head, the femoral head, and the dome of the talus. Osteochondral fragments at
any site and isolated fragments of cortical bone are also vulnerable to
osteonecrosis.
BONE MARROW EDEMA SYNDROME

Bone marrow edema syndrome is an umbrella term that includes the entities of
transient osteoporosis, regional migratory osteoporosis, and reflex sympathetic
dystrophy.7,8 It is characterized by transient, clinically painful marrow edema, in
the absence of trauma, that resolves spontaneously. The pathogenesis of these
conditions remains under debate, but maladaptive activation of the regional
acceleratory phenomenon may play a role. Regional acceleratory phenomenon is
marked by increased rate of bone turnover in response to certain stimuli. The
successful use of bisphosphonates, which reduce bone turnover, in treatment of
bone marrow edema syndrome in some studies supports this theory. Bone
marrow edema syndrome is characterized by focal marrow edema on MRI with
high T2 signal and low T1 signal, corresponding to the area of clinical symptoms
(Figure 27.18). Radiographs are often initially normal but may show
demineralization at 3 to 6 months follow-up. The ankle and hip are common
sites of involvement; when involvement is limited to the proximal femur, this
entity may also be called transient osteoporosis of the hip. Transient osteoporosis
of the hip was initially described in women during the third trimester of
pregnancy but also commonly affects otherwise healthy middle-aged men.
Because imaging features of bone marrow edema syndrome are nonspecific,
clinical history and follow-up imaging play an important role. History of trauma
may be used to differentiate bone marrow edema syndrome from bone
contusion. The presence of subchondral fracture or progression to subchondral
collapse or secondary osteoarthritis excludes bone marrow edema syndrome and
suggests osteonecrosis. Emerging use of dynamic contrast-enhanced MRI
perfusion patterns may also help in differentiating bone marrow edema from
early osteonecrosis.9
•
FIGURE 27.11 A, Posteroanterior radiograph in a patient with early stage Kienbock
disease showing sclerosis within the lunate (arrow) with preserved articular surface.
Note negative ulnar variance (arrowhead). B, Coronal T1 MRI of the same patient
showing lunate marrow edema (arrow).
•
FIGURE 27.12 Posteroanterior radiograph showing advanced Kienbock disease
with lunate sclerosis and subchondral collapse (arrow), rotatory subluxation of the
scaphoid (arrowhead), and radiocarpal osteoarthritis.
•
FIGURE 27.13 Posteroanterior radiograph showing radial shortening osteotomy for
early stage Kienbock disease, with correction of negative ulnar variance.
•
FIGURE 27.14 Anteroposterior radiograph of the shoulder showing humeral head
osteonecrosis. Note crescentic subchondral lucency (arrow) denoting subchondral
insufficiency fracture with subchondral collapse.
•
FIGURE 27.15 Multiple marrow infarcts. A, Radionuclide whole body scan for
evaluation of metastatic disease shows multiple foci of increased activity, including
distal femurs and proximal tibias. B, Radiograph of left femur shows region of
calcification in distal femoral shaft with irregular margins. C and D, Coronal and axial
T2 FS MRI show an extensive intramedullary region of intermediate signal with bright
serpentine margins .
•
FIGURE 27.16 Medullary bone infarcts. A, Coronal T1 MRI shows multiple infarcts
in the femur and tibia with serpentine margins. There has been subchondral collapse
of the medial tibial plateau. B, Coronal T2 FS MRI shows the double line configuration
of the margins of the infarcts.
•
FIGURE 27.17 Calcified marrow infarcts in the femur and tibia.
SICKLE CELL DISEASE

Sickle cell disease is caused by an inherited structural defect in hemoglobin that
leads to red cell dysfunction.10 The radiologic features of sickle cell disease in
bone are the result of bone marrow hyperplasia, vascular occlusion, and
osteomyelitis.11 Hyperplasia of the bone marrow expands the marrow space.
Vascular occlusion results in osteonecrosis. Any portion of any bone may be
involved; frequent sites include the medullary space of long bones, growing
epiphyses, and the hands. Multiple small infarcts sustained over a period of years
may result in sclerotic bones (Figure 27.19). New periosteal bone apposed to
necrotic cortex may result in a double layer of cortex that has been likened to
tram tracks. Involvement of growing epiphyses leads to growth disturbances; if
the femoral head is involved, the pathophysiologic events and sequelae are
indistinguishable from those of Legg-Calvé-Perthes disease. A growth
disturbance in the vertebral body leads to the development of H-shaped
vertebrae (Figure 27.20). Localized infarctions of bone with repair or dystrophic
calcification result in focal areas of bony sclerosis scattered about the skeleton.
Hemosiderosis may follow repeated transfusions of blood (Figure 27.21).
Patients with sickle cell disease have a high incidence of osteomyelitis.
Unlike hematogenous osteomyelitis in other situations, the infection in sickle
cell disease is most frequent at the diaphysis of the long bones, where the
oxygen tension is the lowest. In approximately 50% of cases, Salmonella species
or mixed flora are the causative organisms (their presence is exceedingly unusual
under any other circumstance); the remaining cases are usually caused by
Staphylococcus species. Chronicity and recurrence are common. Osteomyelitis
may be difficult to differentiate from infarction on both clinical and radiologic
grounds: either one can be a complication of the other. The radiographic signs of
osteomyelitis are superimposed on whatever preexisting bone changes are
present from the sickle cell disease.
THALASSEMIA
Thalassemia comprises a group of disorders caused by inherited abnormalities of
globin production that lead to ineffective hematopoiesis and anemia.12 The
defect is in the synthesis of one of the globin chains. There are many types of
thalassemia that are distinguished on the basis of the specific globin chain
affected and the particular molecular defect present. The radiologic findings of
thalassemia in bone result from marrow hyperplasia and marrow space
expansion. These lead to growth disturbances, modeling deformities from
marrow space packing (Figure 27.22), and premature closure of the growth plate.
Extramedullary hematopoiesis is commonly present due to impaired
erythropoiesis. Localized bone infarcts and insufficiency fractures occur
occasionally. Secondary hemochromatosis may follow repeated transfusions of
blood. Bone marrow transplant may be curative and should lead to regression of
the skeletal abnormalities.
•
FIGURE 27.18 Bone marrow edema syndrome in a 63-year-old woman with
atraumatic left hip pain. A and B, Coronal STIR and T1 MRI of the pelvis show patchy
marrow edema within the left femoral head. C and D, Coronal STIR and T1 MRI
4 months later show resolution.
HEMOPHILIA
Classic hemophilia is a bleeding diathesis caused by a sex-linked hereditary
deficiency of coagulation factor VIII. Hemophilia B (Christmas disease) is a
hereditary deficiency of factor IX, and hemophilia C is a hereditary deficiency of
factor XI. The clinical features are similar, and the radiologic manifestations are
indistinguishable.13–15 Approximately 90% of hemophiliac patients have
spontaneous or traumatic hemarthrosis involving the large joints, often in
repeated episodes. The hemarthroses are monoarticular in 70% of cases. The
knee is most commonly affected, followed in frequency by the elbow or ankle
(Figure 27.23). Different joints may become involved in succession, leading to
polyarticular involvement. During an acute bleed, joint effusion and osteoporosis
may be seen. Chronic or repeated hemorrhage leads to synovial hypertrophy and
chronic inflammation. As the abnormal synovium extends across the articular
surface, the cartilage is dissolved, leading to degenerative changes. Subchondral
cyst formation is common, and overgrowth of the epiphyses results from chronic
hyperemia; the younger the age at which these events begin, the more severe the
changes. Secondary degenerative joint disease follows the destruction of the
articular cartilage (Figure 27.24). Intraosseous bleeding and the subsequent
inflammatory reaction that clears the hemorrhage may create radiolucent defects
in bone called pseudotumors. Repeated bleeding into a pseudotumor may cause
it to recur and enlarge, simulating malignancy (Figure 27.25). When such a
pseudotumor is large enough to contain several units of blood, life-threatening
hemorrhage is possible. Many hemophiliacs have been infected with HIV and
viral hepatitis during transfusions with contaminated blood products.
MYELOFIBROSIS
Myelofibrosis with myeloid metaplasia refers to a group of disorders
characterized by progressive bone marrow fibrosis and osteosclerosis with
extramedullary hematopoiesis.16–18 It is a form of chronic leukemia that can
arise de novo (primary myelofibrosis) from the clonal proliferation of myeloid
cells or subsequent to another bone marrow disorder, most commonly
polycythemia vera or essential thrombocythemia. Acute myelofibrosis is a
related but distinct clinical entity that typically arises in the setting of acute
megakaryoblastic leukemia or the acute myeloid leukemia subtype termed
“acute panmyelosis with myelofibrosis.” Diagnosis of primary myelofibrosis is
made based on a combination of bone marrow biopsy (megakaryocytic
proliferation with osteosclerosis), the exclusion of other myeloid neoplasms, and
either the presence of certain clonal immunohistochemical markers (most
commonly JAK2, CALR, MPL) or the absence of nonneoplastic causes of
reactive fibrosis. Treatment of primary myelofibrosis is risk stratified based on
DIPSS Plus score and may range from allogeneic bone marrow transplant and
investigational drugs in high-risk disease to observation in asymptomatic low-
risk disease. Hydroxyurea is commonly prescribed due to the risk of
hyperuricemia in these patients. Leukemic transformation occurs in
approximately 20% of patients within the first decade after diagnosis.
•
FIGURE 27.19 Sickle cell disease with diffuse sclerosis of the humerus from
multiple infarcts.
•
FIGURE 27.20 Sickle cell disease. Sagittal CT showing H-shaped vertebrae
(central, sharply demarcated endplate depressions) of the lower thoracic and upper
lumbar spine.
•
FIGURE 27.21 Sickle cell disease with marrow hemosiderosis. Coronal T1 MRI of
the pelvis shows diffuse low-signal marrow replacement.
•
FIGURE 27.22 Thalassemia. A, Posteroanterior radiograph of the chest showing
generalized bone marrow expansion of the ribs. B, Axial CT shows marked marrow
expansion of the ribs and adjacent paraspinal extramedullary hematopoiesis.
•
FIGURE 27.23 Hemophiliac knee. A and B, Anteroposterior and lateral radiographs
show severe arthropathy and epiphyseal overgrowth.
•
FIGURE 27.24 Hemophiliac knee. A, Coronal T1 MRI shows severe arthropathy of
the medial and lateral compartments of the knee with dysplastic changes. B, Axial T2
FS MRI shows diffuse cartilage loss in the patellofemoral compartment.
•
FIGURE 27.25 Hemophilia with pseudotumor in the pelvis. A, Anteroposterior
radiograph of the pelvis shows a large, expansile, lucent lesion involving the left iliac
wing. B, Axial CT shows heterogeneous attenuation within the mass without
calcification.
•
FIGURE 27.26 Sagittal CT showing diffuse bone marrow sclerosis of the thoracic
spine, sternum, and manubrium in a patient with myelofibrosis.
The most common imaging findings in primary and secondary myelofibrosis
are massive splenomegaly and osteosclerosis of the axial skeleton and
metaphyses of the femurs, humeri, and tibias.18 The osteosclerosis appears as
uniform or geographic areas of hyperdense bone on XR/CT (Figure 27.26) and
as hypointense osseous/marrow signal on all MR sequences (Figure 27.27).
Extramedullary hematopoiesis is most commonly identified in the liver, spleen,
and lymphatic tissue (especially paravertebral). The deposits of extramedullary
hematopoiesis can be masslike, mimicking neoplasms. Acute myelofibrosis will
not typically demonstrate organomegaly or extramedullary hematopoiesis.
LYSOSOMAL STORAGE DISORDERS

Gaucher disease is the most common lysosomal storage disorder, with an
incidence of approximately 1/50 000. Although 3 types of Gaucher disease exist,
only type 1 is relevant to adult radiology. In this autosomal recessive condition,
deficiency of glucocerebrosidase results in the progressive accumulation of
histiocytes laden with glucocerebroside lipids in the bone marrow and other
organs and tissues. Secondary changes in the bone are observed. The classic
radiographic finding is the Erlenmeyer flask deformity, which is undermodeling
of the metaphysis due to marrow space packing (Figure 27.28).19 Additional
common findings include bone infarcts that may occur throughout the skeleton
(Figure 27.29); bilateral femoral head osteonecrosis is particularly characteristic.
Cortical thinning by endosteal erosion as well as osteopenia places patients at
risk for pathologic fractures. After prolonged enzyme replacement therapy with
macrophage-targeted glucocerebrosidase (glucosylceramidase), marrow
composition, bone mass, and bone morphology revert toward normal.
Mucopolysaccharidoses (MPSs) are a group of lysosomal storage disorders in
which the enzymes necessary to metabolize glycosaminoglycans are absent or
malfunctioning. There are different MPS types that are distinguished by the
exact enzyme deficiency, but all of them have a progressively deteriorating
clinical course as the accumulation of unmetabolized glycosaminoglycans
affects the development and function of multiple organ systems. Many patients
with MPS are now living into adulthood, and some enzyme replacement
therapies are in use. The musculoskeletal condition that accompanies MPS is
called dysostosis multiplex and consists of a variety of abnormalities including
short stature, skeletal dysplasia, vertebral anomalies, arthropathies, and joint
contractures.
•
FIGURE 27.27 Sagittal lumbar spine MRI showing generalized decreased signal on
T1 (A), T2 (B), and STIR (C) characteristic of myelofibrosis.
FIGURE 27.28 • Gaucher disease. A, Bilateral AP knee radiographs show

Erlenmeyer flask appearance of the distal femurs. B, Coronal T1 MRI shows diffuse
marrow replacement.
FIGURE 27.29 • Gaucher disease. A, Anteroposterior radiograph showing
Erlenmeyer flask deformity with serpiginous intramedullary sclerosis (arrowhead)
indicating extensive bone infarcts, as well as cortical thinning (arrow); B and C,
Coronal T1 and STIR MRI show T1 hypointense and T2/STIR hyperintense marrow
infarcts (arrows).
References
1. Navarro SM, Matcuk GR, Patel DB, et al. Musculoskeletal imaging findings of hematologic
malignancies. RadioGraphics. 2017;37:881–900.
2. Etienne G, Mont MA, Ragland PS. The diagnosis and treatment of nontraumatic osteonecrosis of the
femoral head. Instr Course Lect. 2004;53:67–85 [PMID:15116601].
3. Beltran J, Herman LJ, Burk JM, et al. Femoral head avascular necrosis: MR imaging with clinical-
pathologic and radionuclide correlation. Radiology. 1988;166(1 Pt 1):215–220 [PMID:3336682].
4. Jose J, Pasquotti G, Smith MK, Gupta A, Lesniak BP, Kaplan LD. Subchondral insufficiency fractures
of the knee: review of imaging findings. Acta Radiol. 2015;56(6):714–719.
5. Arnaiz J, Piedra T, Cerezal L, et al. Imaging of Kienböck disease. AJR Am J Roentgenol.
2014;203(1):131–139.
6. Nealey EM, Petscavage-Thomas JM, Chew FS, Allan CH, Ha AS. Radiologic guide to surgical
treatment of Kienbock’s disease. Curr Probl Diagn Radiol. 2017. pii:S0363–0188(17)30100-7.
doi:10.1067/j.cpradiol.2017.04.012 [PMID:28619441].
7. Singh D, Ferrero A, Rose B, Goldberg A, Cullen N. Bone marrow edema syndrome of the foot and
ankle: mid- to long-term follow-up in 18 patients. Foot Ankle Spec. 2016;9(3):218–226.
8. Korompilias AV, Karantanas AH, Lykissas MG, Beris AE. Bone marrow edema syndrome. Skeletal
Radiol. 2009;38(5):425–436.
9. Geith T, Niethammer T, Milz S, Dietrich O, Reiser M, Baur-Melnyk A. Transient bone marrow edema
syndrome versus osteonecrosis: perfusion patterns at dynamic contrast-enhanced MR imaging with high
temporal resolution can allow differentiation. Radiology. 2016:152665.
10. Piel FB, Steinberg MH, Rees DC. Sickle cell disease. N Engl J Med. 2017;376(16):1561–1573.
doi:10.1056/NEJMra1510865 [PMID:28423290].
11. Kosaraju V, Harwani A, Partovi S, et al. Imaging of musculoskeletal manifestations in sickle cell disease
patients. Br J Radiol. 2017;90(1073):20160130. doi:10.1259/bjr.20160130 [Epub March 10, 2017
PMID:28281830].
12. Aydinok Y. Thalassemia. Hematology. 2012;(17 suppl 1):S28–S31.
doi:10.1179/102453312X13336169155295.
13. Keshava SN, Gibikote S, Doria AS. Imaging evaluation of hemophilia: musculoskeletal approach.
Semin Thromb Hemost. 2015;41(8):880–893. doi:10.1055/s-0035-1564798 [Epub October 19, 2015.
PMID:26479893].
14. Jaganathan S, Gamanagatti S, Goyal A. Musculoskeletal manifestations of hemophilia: imaging
features. Curr Probl Diagn Radiol. 2011;40(5):191–197. doi:10.1067/j.cpradiol.2010.08.001
[PMID:21787985].
15. Kerr R. Imaging of musculoskeletal complications of hemophilia. Semin Musculoskelet Radiol.
2003;7(2):127–136 [PMID:12920650].
16. Tefferi A. Myelofibrosis with myeloid metaplasia. N Engl J Med. 2000;342(17):1255–1265.
17. Arber DA, Orazi A, Hasserjian R, et al. The 2016 revision to the World Health Organization
classification of myeloid neoplasms and acute leukemia. Blood. 2016;127(20):2391–2405.
18. Guermazi A, de Kerviler E, Cazals-Hatem D, Zagdanski A-M, Frija J. Imaging findings in patients with
myelofibrosis. Eur Radiol. 1999;9(7):1366–1375.
19. Katz R, Booth T, Hargunani R, Wylie P, Holloway B. Radiological aspects of Gaucher disease. Skeletal
Radiol. 2011;40(12):1505–1513.
1. What is the characteristic radiographic appearance of early osteonecrosis of the

femoral head?
A. Normal
B. Crescent sign
C. Femoral head sclerosis
D. Femoral head collapse
2. Which condition is associated with the Erlenmeyer flask appearance of the

distal femur?
A. Sickle cell disease
B. Gaucher disease
C. Thalassemia
D. Paget disease
3. Which condition is most commonly associated with extramedullary

hematopoiesis?
A. Sickle cell disease
B. Hemophilia
C. Thalassemia
D. Myelofibrosis
4. Kienbock disease is most closely associated with which bone?

A. Talus
B. Cuboid
C. Scaphoid
D. Lunate

1. A Radiographs are normal in early osteonecrosis.
2. B Erlenmeyer flask appearance is associated with untreated Gaucher disease.
3. C Extramedullary hematopoiesis is most common in thalassemia.
4. D Kienbock disease involves the lunate.
28
Musculoskeletal Ultrasound
Felix S. Chew and Sandra J. Allison
This chapter provides a brief introduction to musculoskeletal sonography for the

beginning resident, but excellent, more detailed resources are available.1–4
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of musculoskeletal ultrasound, the learner will be
able to
1. describe the appropriate imaging approaches and patient positioning,
2. describe the sonographic features, and
3. summarize relevant concepts and knowledge for the following anatomic regions: shoulder,
elbow, wrist, hand and finger, hip, knee, ankle, and foot.
INTRODUCTION
For the less experienced musculoskeletal imager, one approach after placing the
ultrasound transducer on the patient is to identify an anatomic point of reference,
often the surface of an expected underlying bone, and work from there to
identify the structures of interest. Knowledge of musculoskeletal anatomy based
on experience with MRI and CT is applicable, but facility with sonoanatomy
requires the knowledge and skill to understand and visualize anatomy from
multiple and changing points of reference. Comparison with the contralateral
side is often helpful. It is also important to position yourself, the ultrasound
machine, and the patient in such a way that everyone is comfortable; the body
part of interest, the ultrasound probe, and other scanner controls are easily
accessible; and the screen is visible. An accessory flat-panel screen may allow
the patient to view the examination as well.
Sonograms are always displayed with the body surface touching the
transducer at the top. By convention, longitudinal sonograms are oriented with
the proximal aspect to the viewer’s left and the distal aspect to the viewer’s right.
Transverse sonograms are oriented like MRI and CT, as if looking at the patient
from the foot of the bed, an orientation that depends on the location of the
transducer and the side being examined.
The echogenicity of many musculoskeletal structures varies on the relative
direction of the ultrasound beam, a property called anisotropy. When the sound
beam produced by the transducer is not perpendicular to the axis of a structure
that has a parallel internal architecture such as tendons, ligaments, nerves, and
sometimes muscles, there can be artifactual hypoechogenicity, and the structure
may appear as if it has a dark defect. The lack of echoes is a result of ultrasound
waves being reflected away by the structure and not contributing to image
formation. Performing a heel-to-toe maneuver or rocking the transducer to
change the beam angle will restore the expected echogenic appearance, unless
there is an actual hypoechoic abnormality (Figure 28.1). Because many lesions
are hypoechoic with an appearance similar to anisotropic artifact, continuous
adjustment of the transducer is a common scanning technique to determine
which findings are real and which are artifactual. Increased through transmission
is the situation where a structure in the near field transmits sound well because
of relatively uniform composition, resulting in more sound waves penetrating to
deeper structures and contributing to image formation; the far structure will
appear more echogenic than normal. Acoustic shadowing is the situation where
sound waves are blocked by a structure, such as a bone, resulting in no sound
waves penetrating to visualize deeper structures. Compression of structures with
the transducer (sonopalpation) and correlation of specific anatomy with pain,
tenderness, and physical examination increase the information available from the
ultrasound examination. Dynamic scanning while a patient performs maneuvers
to elicit pathology is useful to evaluate a wide variety of musculoskeletal
disorders such as subluxating structures.
A normal tendon has closely packed parallel echogenic fibers. Signs of
tendinosis include thickening of the tendon and heterogeneous echogenicity as
mucoid material separates the normally compact structures. Abnormal tendons
will also become diffusely hypoechoic, and neovascularity may be present in the
surrounding tendon sheaths. Signs of tendon tears include focal hypoechoic
regions, discontinuity, fluid, and absence from the expected location. Tendon
tears commonly occur through underlying tendinosis; therefore signs of
tendinosis often coexist. Hematoma at the site of tendon tears may appear
complex but disorganized, replacing the normal tendon structure. An empty
tendon sheath may also be seen.
Muscles are organized into fascicles of fibers separated by fibroadipose tissue
(called the perimysium) and contained within a fascial envelope, the epimysium.
Muscle fascicles are hypoechoic, whereas the perimysium is hyperechoic. The
epimysium and intramuscular septa are brightly echogenic. The parallel structure
of muscle fascicles may cause anisotropy although to a much lesser degree than
with tendons. Grade I strains may appear as a focal or diffuse hyperechoic
disturbance in the normal structure of muscle. Perifascicle fluid may be present.
Delayed-onset muscle soreness may have the same appearance. Grade II strains
are partial intrasubstance tears, which may demonstrate hypoechoic disruption of
the muscle fascicles, hypoechoic intramuscular fluid collections, and hyperemia
on color Doppler. Grade III strains will have complete discontinuity of the
muscle-tendon structure. Muscle strains generally occur at the musculotendinous
junctions.
FIGURE 28.1 • Anisotropy artifact of the extensor tendon at the proximal

interphalangeal (PIP) joint. There is diffuse edema. As the tendon curves over the PIP
joint, the portion that is perpendicular to the transducer shows the parallel fibers within
(short arrows). The proximal (arrowhead) and distal (long arrow) portions of the
tendon appear hypoechoic from anisotropy, as the tendon curves away from the axis
of the transducer. PP, proximal phalanx; MP, middle phalanx.
Normal fluid found in joints and bursae is anechoic and will be contained by
a capsule. The capsule itself may not be identifiable as a separate structure.
There may be echoes within joint or bursal fluid if debris such as blood clots or
pus is present. Synovitis would appear as hypoechoic thickening of the involved
structure. Color Doppler may show hyperemia in synovitis. Normal bursae may
appear as thin hyperechoic structures in their expected locations, without gross
fluid or more typically not seen at all as they are potential spaces; the presence
of sonographically visible fluid indicates bursitis.
Cortical bone has a highly echogenic interface with soft tissues that appears
as a sharp line on sonograms with complete shadowing of deeper structures.
Fractures may be seen as a discontinuity in the cortical bone or a discontinuity
with an offset, if there is displacement. Surrounding edema, hematoma, or fluid
may be present, as well as pain on sonopalpation. Small, displaced fragments of
bone, such as displaced avulsion fractures, may appear as echogenic structures
with shadowing. There may be surrounding hyperechoic soft tissue edema or
hematoma at a fracture site. Radiography is generally preferred over sonography
for identifying fractures.
SHOULDER ULTRASOUND
The location of shoulder symptoms identified by patients does not correlate well
with actual anatomic sites of pathology; therefore a comprehensive ultrasound
examination is generally preferred to a more focused examination. The patient is
initially seated upright on a stool with the elbow flexed and the hand on the
ipsilateral knee (neutral rotation). The patient may be scanned with the examiner
in front or behind the patient. The examination begins with the transducer at the
front of the shoulder over the humerus. With the transducer transversely oriented
relative to the arm, the lesser tuberosity of the humerus is an excellent landmark.
The bicipital groove and the long head of the biceps tendon may be
demonstrated in transverse and longitudinal views (Figure 28.2). If the tendon is
not within the bicipital groove, it may be torn and retracted or medially displaced
(Figure 28.3). The transducer is then moved medially to visualize the
subscapularis tendon, in longitudinal and transverse views (Figure 28.4).
Externally rotating the arm improves visualization of the subscapularis muscle
belly, and the musculotendinous junctions may be followed to their insertion at
the lesser tuberosity. Some fibers will traverse the bicipital groove as part of the
transverse humeral ligament. Visualization of the acromioclavicular joint is
performed with the transducer at the superior aspect of the acromioclavicular
joint (Figure 28.5). The distal clavicle is thicker than the acromion; therefore its
surface is more prominent. The patient’s hand can then be moved to the back of
the hip, with either the front or the back of the hand touching it (extension and
external rotation, the modified Crass position); this maneuver rotates the top of
the humeral head (HH) and the supraspinatus tendon anterior to the acromion so
that it can be imaged in transverse and longitudinal views (Figure 28.6). On the
longitudinal view, the tendon can be followed laterally to its footprint at the
greater tuberosity (GT). The subdeltoid-subacromial bursa is typically not seen
and closely follows the superior surface of the supraspinatus tendon; it will
extend laterally beyond the supraspinatus footprint to the lateral margin of the
GT. Supraspinatus tendinosis may be evident as thickening and diffuse or patchy
loss of echogenicity (Figures 28.7–28.9). Partial-thickness tears are evident as
focal hypoechoic regions, within the substance of the tendon or on the bursal or
articular surfaces. Large or retracted tears result in the absence of the tendon
(Figure 28.10); often the margins of the torn tendon cannot be identified. With
the arm now held across the front of the body (abduction and internal rotation),
the transducer can be moved to the posterior aspect of the shoulder, just below
the posterior aspect of the acromion, where infraspinatus and teres minor
tendons may be visualized (Figures 28.11 and 28.12), again in transverse and
longitudinal views. The posterior aspect of the glenohumeral joint and
spinoglenoid notch should be visible from this posterior position as well.
•
FIGURE 28.2 Normal long head of the biceps tendon. Anterior shoulder sonogram.
A, Transverse sonogram shows the tendon within the bicipital groove (arrow). The
transverse ligament extends across the tendon. The subscapularis tendon inserts at
the lesser tuberosity (LT). B, Longitudinal sonogram displays the tendon (arrow) as it
descends along the humerus. GT, greater tuberosity.
Calcification in the rotator cuff is hyperechoic with acoustic shadowing; small

flecks of calcification are generally recognizable, but large conglomerate
calcifications may be mistaken for the HH. Subdeltoid-subacromial bursitis may
be evident as bursal fluid and bursal thickening (Figure 28.13). Depending on
how much fluid is present, it may only be present in the dependent portions of
the bursa, which depend on the positioning of the patient. If too much pressure is
applied to the transducer and the walls of the bursa are compressed together,
fluid may be expressed out of the field of view. Dynamic examination of the
shoulder may reveal subacromial impingement of the subdeltoid-subacromial
bursa and supraspinatus tendon.
•
FIGURE 28.3 Biceps dislocation. Transverse sonogram of the right shoulder shows
medial dislocation of the long head of the biceps tendon (arrow). GT, greater
tuberosity; LT, lesser tuberosity; arrowhead indicates bicipital groove.
•
FIGURE 28.4 Normal subscapularis tendon. Anterior shoulder sonogram with the
shoulder externally rotated. A, Transverse. HH, humeral head. B, Longitudinal. LT,
lesser tuberosity.
•
FIGURE 28.5 Normal acromioclavicular joint. Superior shoulder sonogram shows
the joint between the distal clavicle (Cl) and acromion (Ac).
•
FIGURE 28.6 Normal supraspinatus tendon. Anterior shoulder sonogram with the
patient in the modified Crass position. A, Longitudinal sonogram shows the humeral
head (HH), sonolucent articular cartilage, supraspinatus tendon, deltoid musculature,
and subcutaneous tissues. B, Transverse sonogram shows the supraspinatus tendon
coursing over the HH to insert at the greater tuberosity (GT). The subdeltoid-
subacromial bursa extends distally beyond the footprint of the supraspinatus tendon.
•
FIGURE 28.7 Partial rotator cuff tear and tendinosis of a 42-year-old woman with
acute onset of anterior shoulder pain while reaching across her body. A, Long-axis
sonogram shows thickened supraspinatus tendon (arrows) extending across the
humeral head (HH) and inserting at the greater tuberosity (GT). B, Short-axis
sonogram shows the thickened supraspinatus tendon (arrows) with a focal contour
abnormality (arrowhead) overlying a hypoechoic articular surface partial-thickness
tear (*).
Sonography, MRI, and MR arthrography have all been shown in multiple

studies to have good diagnostic accuracy for rotator cuff tears.5,6 A recent meta-
analysis of these modalities for the diagnosis of rotator cuff tears has shown low
or unclear methodological quality of the available studies relative to determining
comparative effectiveness.7 The superiority of one modality over another is
probably dependent on local expertise and individual patient circumstances.
Assessment of other shoulder pathologies such as labral tears and paralabral
cysts (Figure 28.14), the rotator cuff interval, and glenohumeral ligaments may
be accomplished by advanced sonographers, but practically, MRI and MR
arthrography are more likely to demonstrate these structures consistently.
ELBOW ULTRASOUND
The elbow may be visualized from 4 sides, depending on the structures to be
examined. The lateral elbow examination can show the common extensor origin
and deep to that, the radial collateral ligament with the meniscus homologue
(Figure 28.15). Lateral epicondylitis is tendinosis of the common extensor
origin, an overuse syndrome commonly associated with tennis (sometimes called
tennis elbow). On sonography, the tendon origin is thickened, hypoechoic, and
tender to sonopalpation. Tears may be present as well as increased vascularity on
power Doppler. The medial elbow examination can show the common flexor
origin and deep to that, the ulnar collateral ligaments. Medial epicondylitis
(sometimes called golfer’s elbow) is less common than lateral epicondylitis but
has similar sonographic features (Figure 28.16). Tears of the ulnar collateral
ligament, particularly the anterior band, are associated with throwing sports.
•
FIGURE 28.8 Supraspinatus tendinosis. Longitudinal sonogram shows that the
supraspinatus tendon is thickened and diffusely hypoechoic (short arrows), with a
focal region of tendinosis (long arrow). Fluid in the subdeltoid-subacromial bursa is
present in the dependent portion (arrowhead).
•
FIGURE 28.9 Supraspinatus tendon partial tear. Transverse sonogram through the
supraspinatus footprint shows a partial-thickness tear bursal surface of the posterior
aspect of the tendon (arrow). GT, greater tuberosity.
•
FIGURE 28.10 Complete rotator cuff tear of a 62-year-old man with anterolateral
shoulder pain and disability. Right shoulder scanned in position 4. A, Long-axis
sonogram shows absence of the supraspinatus tendon over the humeral head (HH)
and greater tuberosity (GT). The echogenic, thickened subdeltoid-subacromial bursa
(arrow) follows the humeral surface but extends distally beyond the supraspinatus
footprint. B, Short-axis sonogram shows the subdeltoid-subacromial bursa (arrow)
adjacent to the GT and absence of the torn and retracted supraspinatus tendon.
•
FIGURE 28.11 Infraspinatus tendon. Posterior shoulder sonogram. A, Longitudinal.
B, Transverse.
•
FIGURE 28.12 Teres minor tendon and posterior glenohumeral joint. Posterior
shoulder sonogram.
•
FIGURE 28.13 Subdeltoid-subacromial bursitis. Longitudinal sonogram of the right
infraspinatus tendon (*) shows anechoic fluid in the subdeltoid-subacromial bursa
(arrowheads). GT, greater tuberosity; HH, humeral head.
The anterior elbow examination may show the distal biceps tendon and the
brachialis tendon. Biceps tendon tears are much more common because the
biceps mechanism spans 2 joints. However, in a symptomatic patient, when the
biceps is intact, the brachialis tendon should be examined, because symptoms
and injury mechanism are similar. Sometimes, the biceps and brachialis tendons
are easier to demonstrate when the transducer is placed on the medial side of the
elbow and angled to match the course of the distal biceps tendon (Figures 28.17
and 28.18). Fluid around the biceps tendon may indicate bicipitoradial bursitis.
Joint effusion and loose bodies may be seen on the anterior elbow and the radial
nerve.
•
FIGURE 28.14 Spinoglenoid notch paralabral cyst. Longitudinal sonogram of the
shoulder shows a hypoechoic cyst (arrowheads) in the spinoglenoid notch. HH,
humeral head; Sc, scapula.
•
FIGURE 28.15 Normal lateral elbow structures of a 61-year-old man with activity-
related lateral elbow pain. Longitudinal lateral elbow sonogram shows normal
common extensor tendon origin at the lateral epicondyle (LE) and muscles
(arrowheads) coursing distally. The radial collateral ligament (arrow) is deep to the
extensors, and the meniscus homologue (*) protrudes between the capitellum (C) and
the radial head (RH).
The posterior elbow examination includes the triceps tendon and the ulnar
nerve. Triceps tendinosis and ruptures present with the same sonographic
features as those seen in other tendons. The ulnar nerve is typically well seen
sonographically because of its superficial location. Cubital tunnel syndrome and
ulnar nerve entrapment can be diagnosed easily by detecting focal caliber change
at the site of entrapment, hypoechoic thickening of the nerve proximal to the
point of entrapment, and tenderness while scanning the thickened portion of the
nerve. Dynamic scanning while the patient flexes and extends at the elbow may
reveal sources of snapping such as a subluxating ulnar nerve or medial triceps
muscle. Joint effusions and loose bodies may be seen, when present.
WRIST ULTRASOUND
The wrist may be imaged with the patient and examiner sitting across from each
other with both wrists on a table or other suitable surface. This permits right and
left sides to be examined, if comparison is needed. The high-frequency hockey
stick transducer is often recommended because the structures are superficial, and
the skin surfaces available for transducer placement tend to be small. The wrist
may be visualized from 4 sides. The ulnar view is used to examine the extensor
carpi ulnaris tendon (extensor compartment VI), which should rest within the
ulnar groove (Figure 28.19). Dynamic maneuvers may be attempted when there
is a history of snapping or subluxation with change in position; typically,
supination and flexion of the wrist will allow the unstable extensor carpi ulnaris
tendon to dislocate anteriorly out of the ulnar groove (Figure 28.20). The radial
view is used to examine the tendons in extensor compartment I (abductor pollicis
longus [APL] and extensor pollicis brevis [EPB]). De Quervain disease is a
condition of stenosing tenosynovitis involving the abductor pollicis longus and
extensor pollicis brevis (Figure 28.21). These tendons may also be subject to
degeneration and tears (Figure 28.22). The dorsal view is used to visualize the
tendons in extensor compartments II through V. The volar view is used to
visualize the carpal tunnel, the median nerve, Guyon canal, and the ulnar nerve.
Evaluation of the carpal tunnel for carpal tunnel syndrome involves identifying
palmar bowing of the flexor retinaculum, distal flattening of the median nerve,
and enlargement of the nerve proximal to the flexor retinaculum. Peripheral
nerves have hyperechoic superficial epineurium surrounding hypoechoic
neuronal fascicles with interspersed hyperechoic interfascicular epineurium and
thus can be distinguished from muscles, tendons, and ligaments (Figure 28.23).
Ultrasonography may also identify space-occupying lesions within the carpal
tunnel that may cause carpal tunnel syndrome.
Ganglion cysts about the wrist are often symptomatic and may be apparent as
anechoic round or ovoid multilobulated structures. In the postoperative wrist,
impingement of hardware on tendons, particularly the extensor tendons, may be
demonstrated and correlated with symptoms (Figure 28.24).
•
FIGURE 28.16 Medial epicondylitis. Longitudinal sonogram at the medial elbow
shows thickened and diffusely hypoechoic common flexor tendon (arrowheads). ME,
medial epicondyle.
•
FIGURE 28.17 Normal biceps and brachialis tendons. The transducer was placed
on the medial proximal forearm. A, Normal brachialis muscle and tendon (Br). B,
Normal biceps tendon. Hum, humerus, Pr, pronator teres.
•
FIGURE 28.18 Distal biceps tendon tear of a 52-year-old man injured while playing
hockey. He complained of left elbow pain and swelling, and loss of biceps strength.
Anterior sonogram shows the torn distal biceps tendon (Bi) with loss of the normal
organization and structure. Br, brachialis muscle.
•
FIGURE 28.19 Extensor carpi ulnaris (ECU) tendinosis of a 37-year-old man with
ulnar-sided wrist pain. A , Longitudinal sonogram of the right wrist from the medial
side shows thickening and heterogeneity of the ECU tendon (*) at the level of the
carpus (H, hamate; M, fifth metacarpal; U, ulna). B, Short-axis sonogram shows
normal location of the thickened ECU tendon (*) within the ECU groove of the ulna
(U).
•
FIGURE 28.20 Extensor carpi ulnaris (ECU) tendon dislocation of a 22-year-old
man with wrist pain. A, Transverse sonogram of the ulnar side of the wrist shows the
normal ECU tendon (*) located within the ulnar groove (arrowheads). B, With partial
supination and flexion of the wrist, the ECU tendon (*) subluxates anteriorly. C, With
further supination and flexion, the ECU tendon (*) dislocates over the anterior tip of
the now-empty ulnar groove (arrowheads). The tendon relocated with pronation and
extension.
HAND AND FINGER ULTRASOUND

Like the wrist, the hand and fingers may be imaged with the patient and
examiner sitting across a table from each other. Each finger can be imaged from
4 sides. Imaging the ulnar side shows the ulnar collateral ligament complexes.
Imaging the radial side shows the radial collateral ligament complexes. Imaging
the dorsal side shows the extensor tendons. Imaging the volar or palmar side
shows the flexor tendons and the pulleys. The pulley system consists of annular
pulleys (designated A1 through A5) and cruciate pulleys (designated C1 through
C3), also called annular and cruciform ligaments. The pulleys keep the flexor
tendons in close apposition to the volar side of the phalanges, allowing the
transformation of tensile strength from contraction of the forearm muscles to
flexion of the finger joints (Figure 28.25). In activities such as rock climbing, the
entire weight of the body may be held by the joints of 1 or 2 fingers, leading to
overuse injuries.8 Traumatic injuries may also occur with finger dislocations.
Injury to the pulley system results in bowstringing of the flexor tendons, where
the tendons pull away from the volar surface of the phalanges during flexion.
Active attempted flexion while imaging may be necessary to demonstrate
bowstringing. The most common injury is to the A2 pulley at the proximal
phalanx (Figure 28.26). If the injury is isolated to the A2 pulley, the flexor
tendons will bowstring away from the proximal phalanx by no more than 3 mm.
If the injury is more extensive, also involving the A3 or A4 pulleys, the flexor
tendons may separate from the bone by 5 mm or more (Figure 28.27). The
annular pulleys, particularly A2, are the most vulnerable to injury. The A1 and
A5 pulleys and the cruciform pulleys are rarely injured. The A1 pulley, however,
is thickened in the setting of trigger finger. This may be visualized
sonographically given its superficial location and excellent resolution of
ultrasound. Dynamic scan can be performed to assess flexor tendon gliding at
the level of the thickened pulley and observe triggering of the finger.
•
FIGURE 28.21 De Quervain disease. A, Transverse sonogram at the radial styloid
process (Rad) from the lateral side shows thickened, hypoechoic extensor pollicis
brevis (EPB) and abductor pollicis longus (APL) tendons. The surrounding sheath is
also thickened. B, Longitudinal sonogram shows thickened, hypoechoic tendons (*)
with inflamed hyperemic tendon sheath. Dynamic examination would show restricted
tendon movement.
FIGURE 28.22 • Extensor pollicis longus (EPL) tendon rupture. Longitudinal
sonogram shows the distal (short arrow) and proximal (long arrows) retracted ends of
the torn EPL tendon, with the empty segment of the tendon sheath (arrowheads) in
between. 1MC, first metacarpal base; Rad, radial styloid.
Imaging of metacarpophalangeal and interphalangeal joints may show

effusions, synovitis, and erosions (see Figure 15.18). Imaging the joints with
point-of-care ultrasonography has become an important part of clinical
rheumatology and has essentially eclipsed MRI for evaluation and monitoring of
inflammatory polyarthritis patients. Ganglion cysts are commonly found about
the fingers and can be identified using ultrasonography (see Figure 15.19), but
often do not require imaging for diagnosis.
Foreign bodies such as thorns or splinters are common problems in the
fingers. Nonmetallic foreign bodies are usually radiographically occult, but
should be obvious on sonography as a brightly hyperechoic object in the soft
tissues, often with a hypoechoic halo of edema and acoustic shadowing (Figure
28.28).
HIP ULTRASOUND
With the patient in the supine position, the anterior hip can be examined along
the longitudinal and transverse axes relative to the femoral neck. Joint effusion
and synovitis, as well as the anterior bony surfaces, may be demonstrated
(Figure 28.29). The iliopsoas tendon and tendon sheath may be seen. Dynamic
maneuvers may be performed if the complaint is snapping hip syndrome.
Sometimes, the symptomatic structure may be identified in motion by ultrasound
as the patient performs the maneuver that reproduces the snapping sensation.
The acetabular labrum may also be seen, but labral tears may be challenging to
demonstrate by sonography unless a paralabral cyst is identified.
The medial hip region may be examined with the patient in the frog-leg
position. Adductor musculature and iliopsoas tendon may be seen. If athletic
pubalgia is suspected, the pubic bone and attachment of the aponeurosis of the
rectus abdominis and adductor longus may be examined.
With the patient rolled into the decubitus position, the soft-tissue structures
adjacent to the greater trochanter may be examined. Greater trochanteric bursae
and the tendons of the gluteal muscles and tensor fascia lata may be seen. The
gluteus medius tendon inserts on the superoposterior and lateral facets. The
gluteus minimus tendon inserts on the anterior facet. Bursae commonly occur
deep to the gluteus medius tendon (subgluteus medius bursa), deep to the gluteus
minimus tendon (subgluteus minimus bursa), and superficial to the posterior and
lateral facets (trochanteric bursa). An anechoic fluid-filled structure adjacent to
the greater trochanter is an indication of bursitis (Figures 28.30 and 28.31).
Trochanteric bursitis is the most common type of bursitis; subgluteal bursitis is
relatively rare. Tendinosis or tears of the gluteus medius or minimus tendons
may be identified by their location (Figure 28.32). Tendinosis of the gluteus
medius or minimus is a more common cause of trochanteric pain syndrome than
bursitis.9 Calcification may be present within the involved tendons. Iliotibial
band (ITB) abnormalities are also associated with trochanteric pain. Snapping
hip may be the result of the ITB or the gluteus maximus sliding over the greater
trochanter.
•
FIGURE 28.23 Carpal tunnel. A, Transverse sonogram at the carpal tunnel shows
the median nerve (arrow) in cross section. The contents of the carpal tunnel and the
flexor retinaculum (arrowhead) are normal. B, Longitudinal sonogram of the wrist
showing the normal medial nerve (arrow).
•
FIGURE 28.24 Hardware impingement of a 37-year-old man with pain and catching
sensation in his dorsal wrist, 7 months after fracture treatment. A, Lateral wrist
radiograph shows healed distal radius fracture fixed by a volar plate. There are
screws protruding through the dorsal cortex (arrow). B, Longitudinal sonogram shows
the screw tip (arrow) impinging on one of the extensor tendons. Motion of the tendon
correlated with the patient’s symptoms, which resolved after hardware removal.
To image the hamstrings, the patient may be positioned prone with the hips
and knees extended. The semimembranosus has a separate origin on the ischium
that is proximal and lateral to the conjoint tendon of the long head of the biceps
femoris and the semitendinosus (Figure 28.33). It may be easier to follow each
hamstring muscle transversely from origin to insertion than longitudinally
(Figure 28.34). The gluteus maximus, as well as the sciatic nerve, may also be
imaged in this position.
In the setting of total hip replacement, the region should be searched for
extra-articular fluid collections and protruding hardware. In the setting of
possible radiographically occult hip fracture, MRI or CT should generally be
performed rather than ultrasonography.
KNEE ULTRASOUND
Sonography of the knee is useful for focused indications where specific
pathologies are accessible. For a general screening examination for possible
internal derangement or bone pathology, radiography followed by MRI is
usually more appropriate. Imaging the posterior knee can confirm a clinical
diagnosis of Baker cyst. The lesion will be anechoic and arise from the knee
capsule between the semimembranosus tendon and the medial head of the
gastrocnemius and protrudes into the popliteal fossa (Figure 28.35). Because of
this location, Baker cysts are commonly found during Doppler sonography for
possible deep venous thrombosis.
•
FIGURE 28.25 Normal finger flexor tendons. Longitudinal palmar small finger
sonogram showing normal flexor tendons (arrowheads) closely following the surface
of the bones. The thin echogenic structure following the tendons is the tendon sheath.
A, Sonogram at the level of the metacarpal head (MC), metacarpophalangeal joint
(MCP), and proximal phalanx (PP). B, Sonogram at the level of the PP. C, Sonogram
at the level of the middle phalanx (MP) showing the insertion of the flexor tendon at
the distal phalanx (DP). D, Diagram of the annular pulley system. PIP, proximal
interphalangeal; DIP, distal interphalangeal.
•
FIGURE 28.26 Rupture of A2 pulley with bowstringing. A, Longitudinal palmar ring
finger sonogram at the level of the proximal phalanx shows that the flexor tendon (T)
has pulled away from the surface of the proximal phalanx (PP) leaving a fluid-filled
gap (arrowheads) of approximately 2 mm. B, Longitudinal palmar middle finger
sonogram for comparison shows the normal position of the tendon immediately
adjacent to the proximal phalanx.
FIGURE 28.27 • Rupture of the A2, A3, and A4 pulleys with bowstringing.
Longitudinal palmar sonogram of the left middle finger shows marked bowstringing
(approximately 7 mm), indicative of multiple pulley rupture. There is also a volar plate
injury and fluid (*) deep to avulsed plate. MP, middle phalanx; PP, proximal phalanx.
•
FIGURE 28.28 Splinter in the middle finger adjacent to the nail bed. Sonogram of
the distal finger shows an echogenic linear lesion in the soft tissues.
•
FIGURE 28.29 Hip effusion. Longitudinal sonogram of the anterior right hip shows a
joint effusion (arrowheads) over the femoral neck.
•
FIGURE 28.30 Greater trochanteric bursitis. Transverse sonogram of the lateral hip.
Distended fluid-filled bursa at the greater trochanter (GT) (arrow).
FIGURE 28.31 • Greater trochanteric bursitis. Transverse sonogram of the

posterolateral hip shows an anechoic fluid-filled bursa (*). GT, greater trochanter.
•
FIGURE 28.32 Gluteus medius tendinosis. Transverse sonogram of the lateral hip
shows thickened, hypoechoic gluteus medius tendon (arrowheads) adjacent to the
greater trochanter (GT). The hyperechoic band superficial to the gluteus medius is the
iliotibial band.
Sonography of the anterior knee allows evaluation of the infrapatellar and

quadriceps tendons. Like tendons elsewhere, tendinosis involving the quadriceps
mechanism is evident on sonography as thickened, hypoechoic tendons (Figure
28.36). Bursitis may be found between the infrapatellar tendon and the tibia, just
proximal to its insertion, or in the superficial soft tissues in the setting of
prepatellar bursitis. Edema may also be present in the Hoffa fat pad. With the
knee flexed, the articular cartilage over portions of the condyles and the trochlea
may be imaged. MRI is necessary for evaluation of the patellar cartilage. Joint
effusion can be seen around the suprapatellar recess and its lateral and medial
extensions (Figure 28.37).
Imaging the lateral side of the knee can show the lateral collateral ligament
complex, including the ITB (Figure 28.38), the lateral collateral ligament, and
the biceps femoris tendon. Thickening of the ITB with fluid detected deep to the
band at the level of the femoral head may indicate ITB friction syndrome.
•
FIGURE 28.33 Hamstring tendinosis and tear. Longitudinal sonogram of the
posterior upper thigh shows a thickened, hypoechoic semimembranosus tendon
(arrowheads) and a completely torn conjoint hamstring tendon with hematoma (arrow)
and retraction.
The medial aspect of the knee can be scanned to evaluate for medial collateral
ligament (MCL) sprains, which manifest as thickening of the MCL, increased
vascularity on power Doppler imaging, and edema of the surrounding soft
tissues. The pes anserine tendons (sartorius, gracilis, and semitendinosus) and
pes anserine bursa may be seen. The medial patellofemoral ligament can be seen.
Portions of the meniscus may be visible, but the presence or absence of meniscal
tears cannot be determined reliably.
ANKLE ULTRASOUND
The posterior calf and ankle are imaged to evaluate the Achilles tendon. The
tendon should be evaluated from the musculotendinous junction at midcalf to the
insertion at the inferior half of the posterior calcaneus. Athletic injuries tend to
occur at the musculotendinous junction, degenerative changes and injuries more
distally, Haglund disease just superior to the insertion, and enthesopathy at the
insertion itself. The Achilles tendon should be flat or C-shaped and concave
anteriorly, on transverse sonograms, and should have densely packed uniform
parallel fibers on longitudinal sonograms (Figure 28.39). Mucoid degeneration
(Achilles tendinosis) becomes more common in adults as they age and is
especially common in those with diabetes. The tendon becomes thickened (6 mm
or thicker in AP dimension), heterogeneous, and hypoechoic. Comparison with
the contralateral side, if asymptomatic, may be helpful in identifying small
differences in thickness and subtle signs such as increased transmission of sound
through a hypoechoic tendon (Figure 28.40). Doppler may not necessarily show
neovascularity around the tendon because the Achilles tendon does not have a
synovial tendon sheath (Figure 28.41). Tears of the Achilles tendon typically
occur through preexisting disease; most tears are complete rather than partial,
and dynamic examination may be necessary to demonstrate the separation.
Sonographic signs of Achilles tendon tears include interruption of tendon fibers,
loss of tendon volume, alteration of borders, retraction of torn ends, and filling
of the tendon gap by fluid or hematoma (Figures 28.42 and 28.43).
•
FIGURE 28.34 Hamstring tear of a 53-year-old woman with a hamstring tear
sustained while rock climbing. A, Transverse posterior sonogram shows retracted
hamstrings with hematoma (arrow). B, Axial T2 FS MRI shows retracted conjoined
and semimembranosus tendons surrounded by fluid (arrow). AM, adductor magnus;
GM, gluteus maximus; SQ, subcutaneous tissues.
•
FIGURE 28.35 Baker cyst. Transverse sonogram of the left popliteal area shows
anechoic fluid-filled cyst (*) extending between the medial head of the gastrocnemius
(G) and the semimembranosus tendon (SM) into the popliteal fossa.
•
FIGURE 28.36 Infrapatellar tendinosis. The left proximal infrapatellar tendon is
swollen and hypoechoic, measuring 5 mm in thickness. The normal right side, for
comparison, measures 3.4 mm. FP, Hoffa fat pad; P, patella.
FIGURE 28.37 • Knee effusion. Longitudinal sonogram over the anterior

suprapatellar region shows anechoic fluid (*) in the suprapatellar recess, posterior to
the quadriceps tendon (arrowheads) and anterior to the prefemoral fat pad (FP). Pat,
patella.
•
FIGURE 28.38 Normal iliotibial band (arrowheads) insertion at the proximal tibia
shown on lateral longitudinal sonogram of the knee.
•
FIGURE 28.39 Normal Achilles tendon. Posterior ankle longitudinal sonogram
shows insertion (arrowheads) at the calcaneus (C). FP, Kager fat pad.
The posterolateral ankle is where the 2 peroneal tendons may be found

posterior to the lateral malleolus (Figure 28.44). The transducer must be
angulated to follow the bony contours of the ankle, and obtaining good
transducer contact around bony prominences may be challenging. Tendinosis
will be evident as abnormal thickening of the tendon. Split tears of the peroneus
brevis are common and the peroneus longus may displace into the torn portions
of the peroneus brevis so that there may appear to be one large tendon (Figure
28.45), a comma-shaped tendon with the longus in the split tear of the brevis, or
3 separate tendons. This usually occurs where the tendons turn to follow the tip
of the lateral malleolus and course anteriorly. Accessory muscles may be found
adjacent to the peroneal tendons at the level of the posterior malleolus. The
different parts of the lateral collateral ligament are found on the lateral ankle. In
the setting of ankle sprains, the anterior talofibular ligament will appear
thickened and hypoechoic or with a partial or complete defect compatible with
tear. Fluid may be seen deep to and surrounding the ligament. The
calcaneofibular ligament and anterior tibiofibular ligaments may also be
evaluated.
•
FIGURE 28.40 Achilles tendinosis. A, Longitudinal sonogram of the right Achilles
tendon (arrowheads) does not look obviously thickened, but it is hypoechoic and
heterogeneous. Kager fat pad (FP) is more hyperechoic deep to the abnormal tendon
because of increased through transmission of sound through the diseased tendon. B,
Longitudinal sonogram of the asymptomatic left Achilles tendon (arrowheads) is
normal. Kager FP appears more hypoechoic than the right side because more sound
is reflected by the tendon.
•
FIGURE 28.41 Achilles tendinosis. Longitudinal sonogram with Doppler shows
thickened, heterogeneous, hypoechoic Achilles tendon (arrowheads) with increased
through transmission making Kager fat pad (FP) appear bright. Doppler shows no
abnormal flow around the abnormal tendon.
The posteromedial ankle is where the tibialis posterior, flexor digitorum

longus, and flexor hallucis longus tendons are found. The deltoid ligament may
be evaluated on the medial ankle.
The extensor tendons are imaged at the anterior ankle (Figure 28.46). Tibialis
anterior ruptures are easily detected and anterior joint effusions can be
diagnosed.
FOOT ULTRASOUND
Imaging the metatarsophalangeal and interphalangeal joints may be performed in
patients with inflammatory arthritis to document effusions, synovitis, and
erosions, using transverse and longitudinal planes from the dorsal and plantar
aspects.
Imaging of the plantar aponeurosis (also called plantar fascia) for possible
plantar fasciitis may be performed with the transducer on the sole of the heel. In
the prone position, the knee can be flexed to bring the foot into a convenient
position. The normal aponeurosis is flat and compact with parallel echogenic
fibers (Figure 28.47). In plantar fasciitis, the aponeurosis is thickened and
hypoechoic and may have surrounding perifascial edema (Figure 28.48). This
typically involves the medial portion of the central cord of the plantar
aponeurosis but may extend to involve the entire origin.
Imaging for Morton neuroma can be performed by placing the transducer on
the plantar surface of the foot over the lesser metatarsal heads with the toes
dorsiflexed. A Morton neuroma is hypoechoic, noncompressible, and typically
located between the heads of the third and fourth metatarsals. Typically, an
adjacent compressible component is present, representing a fluid-distended
intermetatarsal bursa. On transverse sonograms, the lesion should splay apart the
adjacent metatarsal heads (Figure 28.49). On longitudinal sonograms, the
interdigital nerve may sometimes be demonstrated entering the proximal aspect
of the lesion.
•
FIGURE 28.42 A 74-year-old woman with difficulty walking. Achilles tear is
suspected from clinical examination. A, Longitudinal sonogram of the Achilles tendon
shows complete tear of the tendon with a 2.79 cm gap. The tendon itself is markedly
thickened, indicative of tendinosis. B, Longitudinal sonogram at the Achilles insertion
shows tendinosis.
•
FIGURE 28.43 Acute Achilles tendon rupture. Longitudinal sonogram shows large
unorganized hematoma at the site of the rupture (arrow). The retracted distal stump is
thickened and hypoechoic (*), but the fibrillar structure remains visible.
•
FIGURE 28.44 Normal peroneal tendons. Posterior ankle sonogram. A, Transverse
sonogram shows the peroneus longus tendon (long arrow) posterior to the peroneus
brevis tendon (short arrow) as they curve around the distal fibula (Fib). B, Longitudinal
sonogram shows the peroneus longus tendon (long arrow) and peroneus brevis
tendon (short arrow) coursing posterior to the Fib.
•
FIGURE 28.45 Peroneus brevis tendon split tear. Transverse sonogram of the left
lateral ankle shows a longitudinal split tear of the peroneus brevis tendon (short
arrow) as it courses around the lateral malleolus, giving it a concave shape that
partially envelops the peroneus longus tendon (long arrow).
•
FIGURE 28.46 Tibialis anterior tendinosis. A, Transverse anterior sonogram of the
right ankle shows enlarged and heterogeneous tibialis anterior tendon (**)
(Tib = tibia). B, Sonogram of the contralateral left ankle shows normal tibialis anterior
tendon (*). C, Axial T1 MRI shows enlarged right tibialis anterior tendon (arrow) and
normal left tibialis anterior tendon (arrowhead).
•
FIGURE 28.47 Normal plantar aponeurosis. A and B, Longitudinal sonograms with
the transducer on the sole of the foot shows a normal central slip of the plantar
aponeurosis (arrowheads) arising from the calcaneal tuberosity (Calc) and extending
across the arch. FDB, flexor digitorum brevis.
•
FIGURE 28.48 Plantar fasciitis. Longitudinal sonogram with the transducer on the
sole of the heel shows extensive edema (arrowheads) on the surface of a thickened
and hypoechoic plantar aponeurosis (*). Calc, calcaneus; FDB, flexor digitorum
brevis.
•
FIGURE 28.49 Morton neuroma. A, Transverse sonogram at the level of the
metatarsal heads shows a hypoechoic lesion (arrow) separating the third metatarsal
head (3MT) from the fourth metatarsal head (4MT). The lesion was noncompressible.
B, Longitudinal sonogram at the interspace between the third and fourth metatarsal
heads shows a hypoechoic lesion (arrow) with entering nerve (arrowhead).
References
1. AIUM Practice Parameter for the Performance of a Musculoskeletal Ultrasound Examination.
American Institute of Ultrasound in Medicine; 2017.
http://www.aium.org/resources/guidelines/musculoskeletal.pdf.
2. McNally EG. Practical Musculoskeletal Ultrasound. 2nd ed. Elsevier; 2015.
3. Jacobson JA. Fundamentals of Musculoskeletal Ultrasound. 3rd ed. Elsevier; 2018.
4. Introcaso JH, van Holsbeeck M. Musculoskeletal Ultrasound. 3rd ed. JP Medical; 2016.
5. de Jesus JO, Parker L, Frangos AJ, Nazarian LN. Accuracy of MRI, MR arthrography, and ultrasound in
the diagnosis of rotator cuff tears: a meta-analysis. AJR Am J Roentgenol. 2009;192(6):1701–1707.
doi:10.2214/AJR.08.1241 [PMID:19457838].
6. Roy JS, Braën C, Leblond J, et al. Diagnostic accuracy of ultrasonography, MRI and MR arthrography
in the characterisation of rotator cuff disorders: a systematic review and meta-analysis. Br J Sports Med.
2015;49(20):1316–1328. doi:10.1136/bjsports–2014–094148 [Epub Feb 11, 2015. PMID:25677796;
PMCID:PMC4621376].
7. Lenza M, Buchbinder R, Takwoingi Y, Johnston RV, Hanchard NC, Faloppa F. Magnetic resonance
imaging, magnetic resonance arthrography and ultrasonography for assessing rotator cuff tears in people
with shoulder pain for whom surgery is being considered. Cochrane Database Syst Rev. 2013;
(9):CD009020. doi:10.1002/14651858.CD009020.pub2 [PMID: 24065456].
8. Crowley TP. The flexor tendon pulley system and rock climbing. J Hand Microsurg. 2012;4(1):25–29.
doi:10.1007/s12593–012–0061–3 [Epub January 18, 2012. PMID:23730085; PMCID:PMC3371120].
9. Long SS, Surrey DE, Nazarian LN. Sonography of greater trochanteric pain syndrome and the rarity of
primary bursitis. AJR Am J Roentgenol. November 2013;201(5):1083–1086. doi:10.2214/AJR.12.10038
[PMID:24147479].
1. In the appropriate anatomic location, which sonographic finding indicates

tendon tear?
A. Hypoechoic region
B. Acoustic shadowing
C. Flow on color Doppler
D. Anisotropy
2. Which patient position would be the most advantageous to image the

supraspinatus tendon using ultrasonography?
A. Shoulder abduction
B. Shoulder external rotation
C. Shoulder abduction and external rotation
D. Shoulder extension
3. In the appropriate anatomic location, which sonographic finding is typical of a

ganglion cyst?
A. Hyperechoic region
B. Acoustic shadowing
C. Flow on color Doppler
D. Increased through transmission
4. In the appropriate anatomic location, which sonographic finding is typical of

calcific tendinosis?
A. Hypoechoic region with acoustic shadowing
B. Hyperechoic region with increased through transmission
C. Hyperechoic region with acoustic shadowing
D. Hypoechoic region with increased through transmission

1. A Tendon tears are hypoechoic.
2. D Shoulder extension moves the HH (and supraspinatus tendon) anterior to
the acromion, where it becomes accessible to sonography.
3. D Ganglion cysts are hypoechoic with increased through transmission.
4. C Calcific tendinosis is hyperechoic with acoustic shadowing.
29
Procedures in Musculoskeletal
Radiology
Sean Wo and Jack Porrino
This chapter describes many of the common musculoskeletal procedures we

perform at the University of Washington.
LEARNING OBJECTIVES
At the conclusion of this activity, in the setting of musculoskeletal interventional procedures, the
1. discuss and recommend appropriate procedures,
2. describe indications, contraindications, and complications,
3. describe sequential steps in the performance of procedures, and
4. summarize relevant concepts and knowledge for the following topics: informed consent,
anesthesia and sedation, arthrography, joint aspiration, ultrasound-guided rotator cuff
barbotage, and percutaneous imaging-guided biopsy.
INFORMED CONSENT
Because of the brief and episodic nature of patient encounters in radiology,
obtaining informed consent deserves special attention by the radiologist, who is
often meeting the patient for the first time shortly before an invasive procedure.1
The radiologist has only limited time to establish rapport, educate, reassure, and
obtain written consent, all of which are elements of a complete informed consent
conversation.2 The preprocedure conversation also allows the radiologist to gain
trust and influence patient satisfaction, which is becoming increasingly
important in a climate of changing reimbursement models.3
Details of the procedure should be described in layperson terms, followed by
an explanation of the risks, benefits, and alternatives (Table 29.1). The patient
should be given an explicit opportunity to ask questions and the patient should
indicate adequate understanding of the information presented. The patient, the
radiologist, and a witness should then sign a consent form to document that
consent was given. A statement that informed consent was obtained should be
included in the radiologic report of the procedure and, at some institutions, may
be considered sufficient for documentation of minor procedures, without the use
of a separate consent form.
ANESTHESIA AND SEDATION

Local anesthesia at the skin can be accomplished by raising a subcutaneous
wheal with 1% lidocaine, except in patients with an allergy to lidocaine. Some
authors report that buffering lidocaine solution, which is acidic, with sodium
bicarbonate reduces the burning sensation that occurs as lidocaine is infiltrated
into the skin.4,5 Following the placement of a skin wheal, lidocaine can then be
injected along the anticipated path of the larger needles or devices used for
arthrography, aspiration, and biopsy.
Moderate sedation or general anesthesia is sometimes necessary, particularly
for musculoskeletal biopsies in which the biopsy needle may need to traverse
normal bone to access the lesion, causing substantial pain. For most patients,
small amounts of intravenous fentanyl and midazolam alone or in combination
will provide sufficient sedation for procedures to be completed in relative
comfort.6 A radiology nurse can administer the medications and monitor the
patient under the supervision of the radiologist, who should follow their
institution’s guidelines for the administration of moderate sedation. For general
anesthesia, an anesthesiologist or nurse anesthetist working under the direct
supervision of an anesthesiologist should be present.
IMAGING GUIDANCE FOR JOINT INJECTIONS

Joint injections and aspirations in the large joints can be performed easily using
single-plane fluoroscopic equipment.7,8 A C-arm unit allows greater flexibility in
positioning than a fluoroscopic table. Cross-sectional imaging modalities may be
used for joints that are technically difficult to access using fluoroscopy. CT is the
guidance modality of choice for bone biopsies, and CT fluoroscopy is another
possible option if the equipment is available.9 Ultrasonography is highly
versatile and may be used for localization of soft-tissue lesions or fluid
collections in addition to guidance for intra-articular injections (Figure 29.1).10
Because of high cost and technical limitations, the use of MRI guidance for
musculoskeletal procedures remains very limited.11 Therapeutic joint injections
are used to treat inflammatory and degenerative joint disease and often involve
the administration of corticosteroids and local anesthetics.
Table 29.1 INFORMED CONSENT FOR SINGLE CONTRAST ARTHROGRAPHY AND MR
ARTHROGRAPHY OF A JOINT
Description
A needle is passed through your skin into the (specify) joint. A mixture
of iodinated contrast medium and gadolinium is injected into the joint.
The needle is removed. We take a few X-rays, and then we move you
to the MRI suite for an MRI scan. The fluid we inject will eventually be
removed from your body by your kidneys; the fluid is clear so you will
not notice it. The FDA has not specifically approved gadolinium for
injection into the joints; however, we have found it to be safe and
effective.
Benefits
We are doing this to get images of your (specify) joint that will help us
let your doctor know what might be wrong with your (specify) joint. The
internal structure of the (specify) joint is complex, and some structures
are difficult to see, even with MRI, unless we fill the joint with something
that will make them easier to see.
Risks
Because we are passing a needle from the outside to the inside, there
is a risk of introducing an infection. The risk is very low because we use
sterile technique.
Because we are placing a sharp object into your body, there may be
some pain or discomfort, and there is a risk of bleeding. (Ask for history
of bleeding disorders or blood thinners, including aspirin and
anticoagulants.) We will use local anesthetic at the site of injection to
minimize any pain. The needle is small enough that the risk of
significant bleeding is very low. We will also be avoiding any large
blood vessels.
As with any medication or substance that is injected into your body,
there is always a risk of adverse reaction. Although adverse reactions
to either contrast medium or gadolinium are very rare when injected
into a joint, a reaction is always possible. (Ask for history of drug
allergies and reactions to contrast medium or gadolinium.) Adverse
reactions to contrast medium and gadolinium that have been reported
range from a mild rash to difficulty breathing, heart trouble, and even
death. Most of these reactions occurred following injection into the
bloodstream; we will be injecting your joint, not your veins.
Alternatives
We could do the MRI without injecting contrast and gadolinium, but it
may be less accurate for identifying certain types of disorders, one of
which your doctor thinks you might have.
We could do the MRI after we inject gadolinium into your veins, but it
might be less accurate than the MRI arthrogram for identifying certain
types of disorders, one of which your doctor thinks you might have.
We could not do any procedure at all, but your doctor might not be able
to determine what is wrong with your (specify) joint and therefore might
not be able to treat it properly.
If you do not want us to perform this procedure now, we can always
reschedule it.
Understanding
Do you understand the procedure we are planning to perform on you?
Do you have any questions about it?
Documentation
To document that we have explained this procedure and that you
understand the benefits, risks, and alternatives, please sign this
consent form.
•
FIGURE 29.1 A 53-year-old woman with hallux rigidus. A, Lateral foot radiograph
shows advanced hypertrophic osteoarthritis (arrow) of the first metatarsophalangeal
joint with soft-tissue swelling. B, Sonogram from ultrasound-guided injection shows
intra-articular position of needle (arrow). MT, first metatarsal; PP, first proximal
phalanx.
ARTHROGRAPHY
Arthrography is a procedure in which contrast medium is injected directly into a
joint, followed by imaging. Conventional arthrography and CT arthrography
involve the injection of iodine-based contrast medium with or without air,
followed by radiographic imaging or CT scanning, respectively. MR
arthrography, currently the primary modality for the arthrographic evaluation of
intra-articular pathology, involves the injection of a gadolinium-based solution
under fluoroscopic guidance followed by MRI. Potential complications of
arthrography are listed in Table 29.2. MR arthrography is a very safe procedure,
and serious complications such as infection and anaphylaxis occur with an
incidence of less than 1 in 2000.12,13 Self-limited joint pain occurs in two-thirds
of patients and is the most common adverse reaction after arthrography.14
Occasionally, the referring physician may request intra-articular injection
with bupivacaine, a long-acting anesthetic, for both diagnostic and therapeutic
purposes. If the patient’s symptoms are relieved by the injection, the result
supports intra-articular pathology as a cause of the patient’s symptoms, and the
patient may then be considered for procedures such as total joint replacement.
Continuous intra-articular infusion of local anesthetics, particularly bupivacaine
and lidocaine, has been shown to cause chondrolysis in a dose-dependent
fashion.15 The clinical consequences of single intra-articular bupivacaine
injection remain unclear and are under investigation.16
Contrast Mixture for MR Arthrography

For MR arthrography, a solution of gadolinium-based contrast is injected into the
joint. Notably, the FDA has approved commercially available gadolinium
contrast agents only for intravenous use, and intra-articular injection remains an
off-label indication.17 There have been no reported complications or adverse
reactions attributable to intra-articular gadolinium contrast agent.18 The
gadolinium is cleared from the joints by lymphatics and veins and excreted by
the kidneys. Nephrogenic systemic fibrosis has not been reported to result from
intra-articular gadolinium administration. Nephrogenic systemic fibrosis is dose
dependent, and the whole-body dose of gadolinium is far lower in intra-articular
administration compared with IV administration.18
As a paramagnetic contrast agent, gadolinium is most conspicuous on MRI
using T1-weighted pulse sequences with fat suppression. Adding iodinated
contrast medium to the gadolinium mixture allows the radiologist to document
with certainty the space into which the contrast has been injected and perform a
conventional arthrogram at the same time. The combined effects of field
strength, pulse sequence, and dilution of gadolinium with saline (or lidocaine)
and iodinated contrast are complex, and in vitro studies have yielded variable
results regarding optimal concentration.19–21 In general, the addition of iodinated
contrast causes peak MR signal intensity to occur at a lower concentration of
gadolinium.22 The addition of epinephrine to the mixture will delay the
resorption of the contrast mixture, providing a time period of approximately
1 hour during which the MRI examination can be completed.23,24
Table 29.2 COMPLICATIONS OF ARTHROGRAPHY
Infection
Bleeding
Adverse reaction to contrast medium
Vasovagal syncope
Synovitis
At our institution, we use a 0.5% solution of 0.5 mmol/mL gadolinium for

MR arthrography. We draw 10 mL of 1% lidocaine (with the expectation that the
lidocaine may result in pain relief and subsequently less patient motion during
MRI) into a 20 mL syringe, followed by 10 mL of nonionic contrast into the
same syringe. Next, 0.1 mL of gadolinium contrast agent is drawn into a 1 mL
tuberculin syringe and subsequently injected into the 20 mL syringe. We do not
routinely use epinephrine in the contrast solution. The contents of the syringe
should be gently mixed before use by inverting rather than swirling to avoid
dependent layering.25 It is important to flush any tubing carefully, as small gas
bubbles can mimic intra-articular loose bodies and large gas bubbles can cause
MRI artifacts.8
Shoulder Injection
To access the glenohumeral joint, we use an anterior approach through the
rotator cuff interval under fluoroscopic guidance, which has been shown to be
simple and well tolerated.26,27 However, the technical success of shoulder
injection can be accomplished using multiple guidance modalities and
approaches.28 There is considerable variability among practicing radiologists
regarding needle position.29 We prefer the rotator cuff interval approach, with
the needle aimed at the upper medial quadrant of the humeral head (Figure 29.2).
The rotator interval is a triangular space formed by the borders of the
supraspinatus tendon, the subscapularis tendon, and the base of the coracoid.
Although the long head of the biceps tendon traverses the interval, along with
the biceps pulley (superior glenohumeral and coracohumeral ligaments), external
rotation of the arm is used to clear the tendon laterally.26 An alternative approach
is through the subscapularis tendon, targeting the medial margin of the humeral
head at midglenoid level.8
The patient is positioned supine with the shoulder externally rotated, and a
small sandbag placed on the palm of the hand will remind the patient to keep the
shoulder externally rotated and still.8 The site of injection is localized using
fluoroscopy, and the skin is marked. The skin is then cleansed with povidone-
iodine or chlorhexidine solution, and the shoulder is draped to prepare a sterile
field. It is helpful to ask the patient to look away, as the drape commonly covers
the lower face.
We use a 22-gauge, 3.5-inch spinal needle for shoulder arthrography. The
needle is kept absolutely vertical and inserted straight down through the skin into
the joint. Because the needle bevel tends to steer the needle tip in the direction
away from the side of the bevel, rotating the needle 180° every 5 mm of
advancement helps to keep it straight.30 The needle is advanced until it contacts
the bone. The contrast solution should flow into the joint with no resistance until
it begins to distend. Contrast should flow immediately away from the needle tip
and begin to outline the inside of the joint. If there is resistance to injection or
contrast does not flow away from the needle tip, the needle should be
repositioned before continuing. Reports in the literature regarding the capacity of
the shoulder joint vary widely, ranging from 15 to 35 mL.31–33 At our institution,
we inject a volume of approximately 12 to 15 mL.
•
FIGURE 29.2 Shoulder injection. A, Fluoroscopy shows needle placement in the
medial upper quadrant of the humeral head through the rotator cuff interval. Note
lateral position of needle relative to coracoid process (CC). B, Normal arthrogram in
external rotation. C, Normal arthrogram in internal rotation.
The shoulder should be exercised lightly before imaging. Full-thickness
rotator cuff tears are recognized by contrast flowing into the subdeltoid-
subacromial bursa, outlining the bursal-sided contour of the rotator cuff (Figure
29.3). Identifying and characterizing the site of tear is difficult on conventional
arthrography.
Elbow Injection
Arthrography of the elbow should be performed in conjunction with MRI or CT.
The patient is placed in the prone position on the fluoroscopic table with the arm
above the head. The elbow is flexed 90°, and the thumb is pointed up. The
injection site is made at the articulation of the radial head with the capitellum
(Figure 29.4). A 22-gauge, 1.5-inch hypodermic needle is used for injection into
the elbow joint. When the needle tip is located within the joint capsule, contrast
should flow immediately away from the needle tip and begin to outline the joint.
The capacity of the normal adult elbow has been reported to range from
approximately 5 to 14 mL.31,34 At our institution, the typical volume of injectate
is 3 to 5 mL.
Wrist Injection
MR arthrography of the wrist at 3T with single compartment contrast injection
has been shown to have high sensitivity and specificity for triangular
fibrocartilage complex and intrinsic ligament tears.35 To inject the wrist, the
patient should be positioned supine with the wrist at the side next to the hip. It is
helpful to place a sponge underneath the wrist so that it is slightly flexed and
maintained in a pronated position. We use the same 25-gauge, 1.5-inch
hypodermic needle both to anesthetize the skin and to inject intra-articular
contrast. Under fluoroscopic guidance, the radiocarpal compartment is
approached dorsally, and the needle is aimed as far radial and proximal on the
scaphoid as possible (Figure 29.5). The needle should be inserted vertically until
it contacts the bone, which allows one to gauge needle depth and avoids
injection into the flexor tendon sheaths. On injection, contrast should flow
immediately away from the needle tip and begin to outline the radiocarpal joint.
The capacity of the radiocarpal compartment is approximately 2 to 4 mL.31 If
contrast flows from the radiocarpal joint into the distal radioulnar joint or
midcarpal space, a tear or perforation of the triangular fibrocartilage complex or
intrinsic ligaments is present, respectively (Figure 29.6).35
•
FIGURE 29.3 Shoulder arthrogram shows contrast in the subdeltoid-subacromial
bursa (arrow), indicating a full-thickness rotator cuff tear.
Hip Injection
For injection into the hip joint, we use a 22-gauge, 3.5-inch spinal needle. The
hip capsule extends from the acetabulum to the midportion of the femoral
neck.36 From an anterior approach, a needle inserted vertically anywhere over
the femoral head or proximal neck will allow intra-articular injection; however,
we prefer to insert the needle vertically over the lateral cortex of the proximal
femur at the head-neck junction (Figure 29.7). Although the radiologist should
identify the femoral vessels in all cases, we favor the lateral femoral head-neck
junction because it helps to avoid the medially positioned neurovascular
structures.37 Additionally, needle placement in the middle of the femoral neck
has been shown to substantially increase the risk of extra-articular contrast
extravasation.38 In obese patients, rotation of the patient away from the side
being injected, cranial angulation of the needle, and/or having the patient or
technologist physically pull the pannus away from the involved hip will help to
avoid traversing the abdominal pannus, which potentially violates the
peritoneum.37 Superficial needle placement may result in an injection into the
rectus femoris muscle or tendon passing directly over the hip joint at the
injection site, resulting in linear tracking of contrast.38 When the needle tip is
located within the joint capsule, contrast should flow immediately away from the
needle tip and begin to outline the capsule around the femoral neck. The adult
hip joint holds approximately 10 to 15 mL.31,39,40
Knee Injection
We use a 22-gauge, 3.5-inch spinal needle for injection into the knee. There is
considerable variability among practitioners regarding approach to the knee.29,41
We prefer an anterior approach to the knee. In particular, the anterolateral
approach is well tolerated because it minimizes the distance the needle must
travel through the infrapatellar (Hoffa) fat pad to reach the articular space.42 The
knee is flexed to 90°, and the radiologist’s thumb is placed over the anterolateral
aspect of the lateral tibial plateau to locate the joint space. The needle is then
inserted directly above the palpating thumb to avoid the lateral meniscus, and the
needle is directed posteriorly and slightly medially until it contacts the articular
portion of the lateral femoral condyle (Figure 29.8). The injection should occur
with no resistance, and contrast should flow away from the needle tip, generally
inferiorly along the patellofemoral groove to pool in the knee joint posteriorly. If
contrast stays around the needle tip, the needle is extra-articular and should be
repositioned. The adult knee joint has a large capacity, holding over 100 mL of
fluid according to arthroscopic studies.43,44 In our practice, we inject up to
20 mL of contrast mixture.31
Previously, MR knee arthrography was commonly used for detection of
recurrent meniscal tears in the postoperative setting after partial meniscectomy.45
However, this study is obtained less frequently as of late, for several reasons, and
conventional MRI is overwhelmingly the primary imaging modality obtained in
patients with recurrent knee pain and a history of meniscus surgery at our
institution. Increased signal intensity on MR arthrography in a postoperative
meniscus can be difficult or even impossible to detect without precontrast
images; even when definitely present, the finding is neither fully sensitive nor
specific for recurrent tear.46 Furthermore, MR arthrography can obscure
nonmeniscal internal derangement more easily seen on conventional MRI that
may be the true cause of pain. As an aside, recent literature challenging the
clinical utility of arthroscopic partial meniscectomy has prompted a shift away
from operative management47; how this has influenced the decision to acquire an
MR arthrogram in the patient following partial meniscectomy with recurrent
knee pain is unclear.
Ankle Injection
We use a 22-gauge, 3.5-inch spinal needle via an anterior approach for injection
into the tibiotalar joint. The dorsalis pedis artery is identified via palpation, and
the site of injection is chosen lateral to this. The foot is plantar flexed to open up
the anterior aspect of the ankle joint. Fluoroscopic guidance in the lateral
projection can be used to follow the needle to the joint (Figure 29.9). The
injection should occur without resistance with contrast flowing away from the
needle tip and pooling initially in the dependent portion of the joint. We inject 8
to 10 mL contrast mixture into the tibiotalar joint, which holds up to 20 mL on
average.31,48
Foot Injection
We use a 25-gauge hypodermic needle of appropriate length (1.5-inch length is
adequate for most situations) for injection of foot joints. Our most common
request is for injection of the posterior facet of the subtalar joint, which we
prefer to perform under CT guidance using a lateral approach (Figure 29.10).
The patient is positioned prone or decubitus with the knee flexed and the ankle
in neutral. We use fluoroscopic guidance for the other foot joints. Over the
midfoot, care should be taken to avoid the dorsalis pedis artery. The
talonavicular joint communicates with the anterior and middle subtalar facets (as
components of the acetabulum pedis) and with the calcaneal-cuboid joint (as
components of the Chopart joint), so all of those may be accessed from the
dorsal approach over the head of the navicular (Figure 29.11). The Lisfranc joint
has 3 separate compartments: the first tarsometatarsal (TMT) joint is separate;
the second and third TMT joints are together; and the fourth and fifth TMT joints
are together. All of these may be accessed from the dorsal surface (Figure
29.12). The X-ray beam should be aligned tangential to the joint surface, and the
midfoot may be plantar flexed over a towel to help open the joints. The
metatarsophalangeal joints may also be accessed from the dorsal surface. The
extensor tendon may be avoided by entering the joint off-center (Figure 29.13).
•
FIGURE 29.4 Elbow injection. A, Fluoroscopy shows the needle insertion site
(arrow) using a lateral approach. B, Lateral and C, anteroposterior elbow arthrogram
show normal distribution of contrast.
JOINT ASPIRATION
Joint aspiration (or arthrocentesis) under fluoroscopic guidance is commonly
performed for suspected septic arthritis or characterization of crystal arthropathy.
To avoid the significant morbidity and mortality associated with septic arthritis,
any monoarticular arthritis should be considered infectious until proven
otherwise. A larger needle (20- to 18-gauge) is used than a typical one for joint
injection because pus and normal synovial fluid are more viscous than contrast
medium.49 The approach is similar to that used for arthrography or injection. An
acutely infected joint will typically produce bloody or grossly purulent fluid that
is under pressure. If no fluid can be aspirated, the intra-articular position of the
needle tip can be confirmed with the injection of a small amount of iodinated
contrast medium. The joint should be irrigated with nonbacteriostatic
(preservative-free) saline and the saline aspirated. For a large joint, inject 10 mL
of saline and reaspirate as much as possible. Any material aspirated from a joint
in the setting of suspected infection should be delivered to the microbiology
laboratory for Gram stain, aerobic and anaerobic bacterial cultures, wet prep and
fungus culture, and acid-fast stain and mycobacterium culture.
•
FIGURE 29.5 Radiocarpal wrist injection. A, Fluoroscopy shows needle (arrow)
placement just distal to the radius. B, Wrist arthrogram shows normal distribution of
contrast. Contrast pools dependently at the distal scaphoid (long arrow) and
pisotriquetral joint (short arrow).
•
FIGURE 29.6 Wrist arthrogram demonstrating contrast passing into the distal
radioulnar joint (arrow), indicating tear of the triangular fibrocartilage complex.
Inability to access the joint without traversing inflamed or infected superficial

tissues is widely considered to be an absolute contraindication to joint
aspiration.49 In vitro studies have shown that needles used for aspiration can
translocate sufficient bacteria from overlying cellulitis to cause septic arthritis.50
However, proving this phenomenon in the clinical setting would require
aspiration of sterile synovial fluid through an area of cellulitis followed by
aspiration through uninvolved skin demonstrating joint infection.51 Although
avoiding obviously infected tissue such as an abscess is important, the risk of
inoculation may not outweigh the cost of delay in initiation of appropriate
therapy when traversing cellulitis in the opinion of the ordering clinician. The
practice patterns of musculoskeletal radiologists remain under investigation, and
the decision to proceed with aspiration in this setting should be discussed in
conjunction with the ordering clinician.
Hip Arthroplasty Aspiration

The postreplacement hip joint is the most commonly requested site of
arthrocentesis at our institution. We prefer an anterior approach with the needle
directed on a shallow angle toward the lateral edge of the femoral head or
proximal neck component, which avoids radiographic overlap and allows for
better visualization of the needle’s path (Figure 29.14).37 When the needle tip
contacts the metal of the prosthesis, it is in the joint. The hip joint pseudocapsule
following hip replacement will extend from the bony portion of the acetabulum
to the bony portion of the femur, encompassing the entire exposed metal portion
of the prosthesis.52 If a joint effusion is present, joint fluid can be aspirated with
the needle positioned anywhere along the exposed femoral component.
However, in the absence of effusion, the capsule may be tightly applied to the
femoral component, and it may be necessary to advance the needle posteriorly
into a more dependent portion of the pseudocapsule.53 An additional aid once the
needle is in place is to flex the hip, tightening the posterior capsule and
increasing the redundancy of the anterior capsule. Fluid may also be shifted
more anteriorly within the joint, in better range of the needle. In patients with
Girdlestone (resection) arthroplasty, placement of the needle at the midpoint of
the intertrochanteric line has been shown to be optimal for aspiration.54
•
FIGURE 29.7 Hip injection. A, Fluoroscopy shows the instrument pointing to the
anterior injection site at the lateral femoral head-neck junction. B, Hip arthrogram
shows the normal distribution of contrast.
ULTRASOUND-GUIDED ROTATOR CUFF BARBOTAGE

Calcific tendinosis of the shoulder is usually a self-limited condition
characterized by worsening pain and range-of-motion limitation during its final
resorptive phase.55 Although conservative therapy with NSAIDs is often
sufficient, patients with severe or persistent symptoms may be referred for more
invasive treatment. Ultrasound-guided needle irrigation and aspiration of rotator
cuff tendons (Figure 29.15), also known as barbotage, has an overall minor
complication rate of 7% and no reports of long-term disability.56 Barbotage has
been shown in both nonrandomized and randomized controlled trials to have
superior efficacy compared with conservative medical therapy and subacromial
corticosteroid injection.57,58 However, randomized trials comparing barbotage
with extracorporeal shock wave therapy and arthroscopic excision remain
lacking.
Ultrasound guidance is preferred over fluoroscopy for better visualization of
soft tissue and the slurrylike calcium hydroxyapatite deposits that are
characteristically seen in the resorptive phase of calcific tendinosis.59 There is
considerable variation among institutions and practitioners with regard to the
specific techniques used for barbotage. Published variations include needle sizes,
which range from 15-gauge to 25-gauge, single- versus double-needle irrigation
system, and number of passes that can be safely made through the
calcification.10
PERCUTANEOUS CT-GUIDED BIOPSY

Percutaneous CT-guided musculoskeletal biopsy is commonly indicated for
histopathologic diagnosis of a neoplasm or microbiologic diagnosis of an
infection. Compared with open surgical biopsy, percutaneous biopsy is less
invasive and has a lower risk of complications.60 Image guidance also allows
avoidance of cystic and necrotic areas that may produce false-negative results.
Overall diagnostic yield ranges from 70% to 92%, and overall accuracy ranges
from 71% to 93%.61–70 Some authors report that biopsy of metastatic lesions has
a higher yield than primary tumors, whereas others report similar yields.62,63
Potential complications of percutaneous needle biopsy are listed in Table 29.3.
Serious complications such as bleeding and infection are rare, occurring in 1% to
2% of patients.62,65 In general, we use coaxial technique because it allows
multiple samples to be obtained through a single cannula, reducing morbidity
and radiation exposure.
Soft-Tissue Lesions
Because of the nature of musculoskeletal soft-tissue lesions, pathologists at our
institution prefer core needle biopsy (CNB) over fine needle aspiration (FNA)
for diagnostic accuracy.71 We perform FNA only when CNB cannot safely
access the biopsy target. We use the side-cutting, semiautomated Temno
Evolution needle (CareFusion, Waukegan, IL) for core biopsies (Figure 29.16).72
This needle is placed coaxially through an introducer sheath and available in
various lengths and diameters, ranging from 14-gauge to 20-gauge, although we
obtain a 14-gauge core whenever possible. For FNA, we prefer a 22-gauge
Chiba needle, typically used coaxially through a 19-gauge Chiba needle or an
18-gauge Franseen needle. The 22-gauge needle should be 5 cm longer than the
larger gauge outer needle to allow adequate throw. The Franseen needle is a
front-cutting core biopsy needle with a stylet that has a triangular cutting tip and
a cannula that has 3 cutting teeth.72 Ultrasonography has become our preferred
mode of imaging guidance for soft-tissue biopsy.
Bone Lesions
Similar to soft-tissue lesions, we perform CNB instead of FNA whenever
possible. Sclerotic lesions or lytic lesions protected by intact cortical bone
require a bone-cutting needle for access. We use 3 coaxial biopsy systems: the
Bonopty (AprioMed, Londonderry, NH), the Madison (Laurane Medical,
Westbrook, CT), and the Arrow OnControl Powered Bone Lesion Biopsy
System (Teleflex, Morrisville, NC), all of which produce bone fragments that are
compacted to resemble a core. The Bonopty Penetration Set is a 15-gauge drill
with an eccentric tip allowing it to cut a larger hole that permits the passage of
the 14-gauge cannula.73 This arrangement allows one to perform a biopsy
through any thickness of bone, limited only by the length of the drill. The
Bonopty Biopsy Set is a front-sampling needle that is placed through the
penetration cannula.73 The Madison kit contains a cannula with a trocar-type
stylet, which may be replaced with a drill when advancing the cannula through
dense cortical bone.74 The Madison kit contains an 11- or 13-gauge trephine-tip
biopsy needle that is placed coaxially through the introducer cannula (Figure
29.17). The OnControl device is a battery-powered driver coupled with a
trephine needle that reduces procedure time for sclerotic lesions (Figure 29.18).
Occasionally, we will use a Temno Evolution biopsy needle placed coaxially
through the Bonopty or Madison cannula for lytic bone lesions refractory to
sampling with the Bonopty or Madison needles. As a last resort, we may obtain
FNA using a Chiba needle placed coaxially through the cannula, although
obtaining a diagnostic specimen is less reliable.
FIGURE 29.8 • Knee injection. A, Fluoroscopy shows needle tip position for
anterolateral approach. B, Anteroposterior and C, lateral arthrogram show normal
distribution of contrast.
•
FIGURE 29.9 Ankle injection (different ankles). A, Anterior needle (arrow) approach
under lateral fluoroscopy. B, Anterior needle (arrow) approach under anteroposterior
fluoroscopy.
•
FIGURE 29.10 Subtalar joint injection under CT guidance with the patient in the
prone position.
FIGURE 29.11 • Talonavicular joint injection showing contrast entering the

acetabulum pedis (long arrow) and the calcaneocuboid joint (short arrow).
•
FIGURE 29.12 Injection of second tarsometatarsal joint. C2, middle cuneiform; M2,
second metatarsal.
•
FIGURE 29.13 Injection of second metatarsophalangeal joint. 1, great toe; 2,
second toe; 3, third toe.
•
FIGURE 29.14 Arthrocentesis before (A) and after (B) injection of contrast in the
setting of hip replacement.
•
FIGURE 29.15 A 33-year-old woman with new onset left shoulder pain attributed to
calcific tendinosis of the left infraspinatus tendon. Frontal radiograph of the left
shoulder with internal rotation (A) demonstrates calcific tendinosis of the infraspinatus
tendon (arrow). Longitudinal grayscale ultrasound image at the left infraspinatus
tendon (B) demonstrates a well-demarcated echogenic focus of calcium within the
tendon (outlined by markers). Longitudinal grayscale ultrasound image (C)
demonstrates an 18-gauge needle (arrow) within the calcium (asterisk) during
barbotage procedure.
Table 29.3 COMPLICATIONS OF PERCUTANEOUS NEEDLE BIOPSY
Infection
Bleeding
Nerve root injury
Pseudoaneurysm
Vasovagal syncope
Complex regional pain syndrome (reflex sympathetic dystrophy)
Tumor seeding along needle tract
Failure to obtain a diagnosis
•
FIGURE 29.16 Core biopsy of right subscapularis soft-tissue lesion using the
Temno Evolution needle. The biopsy slot (arrow) is visible.
The needle path should be planned in conjunction with the orthopedic

surgeon who may be performing a tumor resection. There is a low but definite
risk of recurrence along the biopsy tract because of iatrogenic seeding.75–78 As a
result, the biopsy tract and surrounding tissues are often resected along with the
tumor, and care should be taken to avoid crossing more than 1 anatomic
compartment whenever possible.79 For long bones, the preferred approach is
generally orthogonal to the cortex of the bone, avoiding neurovascular structures
and joints, and taking the most direct route.
•
FIGURE 29.17 Core biopsy of right iliac lesion using the Madison needle system.
The cutting needle (long arrow) protrudes beyond the sheath (short arrow).
The specific procedure for bone biopsy will vary by the type of coaxial device
used. In general, the patient is positioned in the scanner, and radiopaque
adhesive localization grid is placed on the skin overlying the region of interest.
The skin is then thoroughly cleaned and anesthetized along with the soft tissues
along the biopsy tract down to the periosteum. A layer of anesthetic should be
deposited adjacent to the periosteum. Rescanning the patient with the anesthetic
needle in place will confirm trajectory and location. A skin nick large enough to
accommodate the introducer cannula is made using the full diameter (5 mm) of a
number 11 scalpel blade. With the stylet in place, the cannula is advanced
through the skin incision under CT guidance and directed to the lesion. The
cannula is advanced with a twisting motion over the stylet until it is firmly
seated in cortical bone close to the lesion. The stylet is then exchanged for a
bone biopsy needle, which is then advanced into the lesion itself. For trephine-
type biopsy needles, the needle is advanced by clockwise rotation with firm,
steady pressure against the bone. The trephine needle has a tendency to “walk”
or change in position as the initial rotations are made, so care should be taken to
maintain the position of the introducer cannula as the trephine needle is rotated.
Once the trephine begins to cut into the bone, it becomes stable and greater
pressure can be used. The position of the needle should be periodically checked
by CT. The needle should be periodically withdrawn and the plug of bone
pushed out using the blunt obturator. If the bone plug is impacted in the needle,
it has a tendency to pop out of the needle suddenly and possibly ricochet out of
the sterile field. Replacing the stylet between biopsy passes decreases the chance
of bleeding. After the biopsy is complete, the stylet should be reinserted into the
needle guide and the entire instrument removed. A postbiopsy scan should be
done to document the biopsy site and identify complications.
FIGURE 29.18 • Core biopsy of iliac wing using the OnControl system. A,
Localization CT shows diffuse sclerotic marrow abnormality. B, Biopsy CT shows the
position and trajectory of the needle. C, Postprocedure CT shows the biopsy tract
(arrow).
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1. Which procedure may be performed by radiologists to treat calcific rotator cuff

tendinosis?
A. Arthrocentesis
B. Biopsy
C. Barbotage
D. Arthrography
2. Which of the following is an element of informed consent?

A. Marking of body part with indelible ink
B. Confirmation of the patient’s date of birth
C. Opportunity for the patient to ask questions
D. Checking expiration date of medications
3. For MR arthrography, what is the recommended concentration of gadolinium

in the solution injected into the joint?
A. 0.5%
B. 5%
C. 25%
D. 50%
4. During arthrography, which of the following indicates that the tip of the needle
may not be intra-articular and should be repositioned before continuing?
A. Contrast outlining the joint
B. Resistance to injection
C. Free flow of contrast away from needle tip
D. Aspiration of synovial fluid

1. C Barbotage is the name of the procedure to treat calcific tendinosis.
2. C Informed consent includes the opportunity for the patient to ask questions.
However, the other options should also be performed.
3. A We use a concentration of 0.5%.
4. B Resistance to injection indicates the needle tip should be repositioned.
SELF-ASSESSMENT EXAM
SELF-ASSESSMENT QUESTIONS
1. Which fracture morphology is demonstrated by this radiograph of the tibial

shaft?
A. Spiral fracture
B. Avulsion fracture
C. Oblique fracture
D. Transverse fracture with butterfly fragment
2. Which biomechanical mechanism of loading would be most closely

associated with the findings in this radiograph of the thigh?
A. Compression
B. Tension
C. Torsion
D. Bending
3. Which descriptor would best apply to a fracture of the femur caused by a
gunshot wound?
A. Pathologic
B. Stress
C. Insufficiency
D. Open
4. Based on this radiograph of the shoulder of a trauma patient, what is the

most likely diagnosis?
A. Anterior shoulder dislocation
B. Posterior shoulder dislocation
C. Anterior glenoid rim fracture
D. Hill-Sachs lesion
5. Based on these lateral (A) and posteroanterior (B) radiographs of the wrist,
what is the most likely diagnosis?
A. Scaphoid waist fracture
B. Rotary subluxation of the scaphoid
C. Perilunate dislocation
D. Midcarpal dislocation
6. Which eponym is most closely associated with an apex posterior fracture of
the proximal ulnar shaft and posterior dislocation of the radiocapitellar joint?
A. Essex-Lopresti
B. Galeazzi
C. Monteggia
D. Pellegrini-Stieda
7. Based on this anteroposterior (AP) radiograph of the hip, what is the most
likely diagnosis?
A. Impacted subcapital femoral neck fracture
B. Displaced transcervical femoral neck fracture
C. Three-part intertrochanteric fracture
D. Intertrochanteric-subtrochanteric fracture
8. Based on this lateral radiograph of the ankle, what is the most likely
diagnosis?
A. Lateral malleolar fracture
B. Talar neck fracture
C. Medial malleolar fracture
D. Calcaneal fracture
9. An avulsion fracture of the lateral margin of the tibial plateau is most closely
associated with which ligamentous injury?
A. Anterior cruciate ligament tear
B. Posterior cruciate ligament tear
C. Medial collateral ligament tear
D. Lateral collateral ligament tear
10. Which stage of fracture healing is shown in this radiograph of the humerus?
A. Primary
B. Inflammatory
C. Reparative
D. Remodeling
11. What is the best designation for the screw shown in this radiograph of the
ankle?
A. Compression
B. Locking
C. Tapered
D. Headless
12. Which radiographic feature is most closely associated with hardware
loosening?
A. Soft-tissue swelling
B. Periosteal reaction
C. Change in position
D. Surrounding sclerosis
13. Based on these sagittal (A) and coronal (B) PD FS MRI of the knee, what is
the best diagnosis in this patient with knee pain?
A. Lateral meniscus, radial tear
B. Medial meniscus, radial tear
C. Lateral meniscus, bucket handle tear
D. Medial meniscus, bucket handle tear
14. Based on this axial T2 FS MRI of the knee, what is the best diagnosis in this
patient with knee pain?
A. Anterior cruciate ligament tear
B. Posterior cruciate ligament tear
C. Transient lateral patellar dislocation
D. Transient medial patellar dislocation
15. Which bone bruise pattern is most closely associated with isolated tears of
the posterior cruciate ligament?
A. Posterior tibia
B. Anterior tibia
C. Medial femoral condyle and medial tibial plateau
D. Lateral femoral condyle and posterior tibia
16. Based on this coronal T1 MR arthrogram image, which rotator cuff tendon is
torn?
A. Subscapularis
B. Supraspinatus
C. Infraspinatus
D. Teres minor
17. Based on this sagittal T2 FS MRI, which muscle has abnormal high T2
signal intensity suggestive of acute denervation atrophy?
A. Subscapularis
B. Supraspinatus
C. Infraspinatus
D. Teres minor
18. Which portion of the glenoid labrum is most subject to normal anatomic
variation?
A. Anterior-superior
B. Anterior-inferior
C. Posterior-superior
D. Posterior-inferior
19. Which structure is indicated by the arrows in this coronal MRI of the elbow?
A. Common extensor tendon
B. Common flexor tendon
C. Medial collateral ligament
D. Lateral collateral ligament
20. Sagittal PD FS MRI in a patient with pain following elbow trauma a few
days earlier. What structure is indicated by the arrow?
A. Meniscus homologue
B. Posterior fat pad
C. Anterior recess
D. Sublime tubercle
21. On MR arthrography of the elbow, what is the meaning of the T-sign?
A. Partial tear of the ulnar collateral ligament
B. Partial tear of the radial collateral ligament
C. Partial tear of the common flexor origin
D. Partial tear of the common extensor origin
22. What is the most likely diagnosis in this coronal T1 MRI of an elderly
woman?
A. Osteonecrosis
B. Intertrochanteric fracture
C. Osteoarthritis
D. Femoral neck fracture
23. Labral tear on hip MRI on radial imaging. Where is the tear?
A. Anterior labrum
B. Superior labrum
C. Posterior labrum
D. Inferior labrum
24. In a patient with negative radiographs, in which circumstance is MR
arthrography of the hip most likely to provide diagnostic information beyond
standard MRI?
A. Suspected osteonecrosis
B. Suspected fracture from fall
C. Suspected stress fracture
D. Suspected labral tear
25. Based on this coronal T1 MRI of the wrist, what is the most likely diagnosis?
A. Scaphoid waist fracture
B. Triangular fibrocartilage complex tear
C. Kienbock disease
D. Lunotriquetral dissociation
26. Based on this coronal T2 FS MRI, what is the best diagnosis?
A. Kienbock disease
B. Scaphoid fracture
C. Ulnar impaction syndrome
D. Scapholunate dissociation
27. The ulnar nerve crosses the volar aspect of the carpus in closest proximity to
which of the following bones?
A. Scaphoid
B. Trapezium
C. Capitate
D. Pisiform
28. Based on this short-axis PD FS MRI of the forefoot in a young man, what is
the best diagnosis?
A. Stress fracture
B. Osteomyelitis
C. Bizarre parosteal osteochondromatous proliferation
D. Morton neuroma
29. Based on this axial T1 MRI of the ankle, which abnormal tendon is indicated
by the arrow?
A. Peroneal brevis
B. Tibialis posterior
C. Flexor digitorum longus
D. Flexor hallucis longus
30. Which ankle tendon normally follows a course that takes it immediately
posterior to the talus?
A. Peroneus brevis
B. Flexor digitorum longus
C. Flexor hallucis longus
D. Tibialis posterior
31. Based on this radiograph of the proximal humerus, which type of tumor is
most likely?
A. Giant cell tumor
B. Cartilage-forming tumor
C. Osteoid-forming tumor
D. Simple bone cyst
32. Which descriptor is most closely associated with the appearance shown on
this axial CT of the femur?
A. Onion skin
B. Ground glass
C. Sunburst
D. Rings-and-arcs
33. Which radiographic feature is characteristic of a nonaggressive solitary bone
lesion?
A. Thin sclerotic margin
B. Layered periosteal reaction
C. Cortical penetration
D. Matrix mineralization
34. Based on this axial CT scan of the proximal leg in a 27-year-old man, what is
the most likely diagnosis?
A. Enchondroma
B. Osteochondroma
C. Chondrosarcoma
D. Osteosarcoma
35. Based on the shoulder radiograph (A) and the axial T2 FS (B) and T1 FS Gd
(C) MRI, what is the most likely diagnosis?
A. Simple bone cyst
B. Aneurysmal bone cyst
C. Fibrous dysplasia
D. Enchondroma
36. Which bone lesion characteristically extends to the subchondral bone in
skeletally mature patients?
A. Osteosarcoma
B. Enchondroma
C. Brodie abscess
D. Giant cell tumor
37. Based on this gadolinium-enhanced coronal T1 FS MRI in a 44-year-old
woman, what is the most likely diagnosis?
A. Chondrosarcoma
B. Osteosarcoma
C. Giant cell tumor
D. Plasmacytoma
38. In a 49-year-old man with right hip pain, based on the AP radiograph (A) and
axial T2 FS (B) and contrast-enhanced axial T1 FS (C) MRI, what is the
A. Chondrosarcoma
B. Osteosarcoma
C. Lymphoma
D. Plasmacytoma
39. Which malignant bone tumor occurs most frequently in the tibial shaft?
A. Chordoma
B. Osteosarcoma
C. Chondrosarcoma
D. Adamantinoma
40. The pattern of abnormality in this whole-body Tc–99m radionuclide bone
scan of a 57-year-old woman suggests which diagnosis most strongly?
A. Paget disease
B. Hypertrophic osteoarthropathy
C. Metastatic disease
D. Osteomyelitis
41. What is the most important diagnosis suggested by the findings on this AP
hip radiograph of a 70-year-old man?
A. Metastatic prostate cancer
B. Osteoarthritis
C. Fracture from ground-level fall
D. Bisphosphonate-related insufficiency fracture
42. Metastases to bone are least likely to be found in which anatomic site?
A. Spine
B. Pelvis
C. Femur
D. Foot
43. Based on the findings on this lateral knee radiograph of a 60-year-old man
with a posterior knee mass, what is the most likely diagnosis?
A. Tumoral calcinosis
B. Loose bodies in a Baker cyst
C. Synovial sarcoma
D. Hemangiomas with phleboliths
44. Based on the axial T2 FS (A) and T1 (B) MRI, what is the most likely
diagnosis in a 54-year-old woman?
A. Pleomorphic sarcoma
B. Liposarcoma
C. Lipoma
D. Muscle atrophy
45. In the general population above the age of 30 years, are primary bone
sarcomas more or less common than primary soft-tissue sarcomas?
A. Bone sarcomas are more common
B. Equal incidence
C. Primary soft-tissue sarcomas are more common
46. A detail of a hand radiograph shows 2 fingers, one of which demonstrates
soft-tissue swelling. Based on the morphology of the swelling, what is the
leading differential diagnosis?
B. Septic arthritis
D. Osteoarthritis
47. What is the best diagnosis based on this AP radiograph of the shoulder?
B. Psoriatic arthritis
C. Osteoarthritis
D. Calcium pyrophosphate dihydrate deposition disease
48. Which type of polyarticular arthropathy typically involves the first
carpometacarpal joint?
B. Psoriatic arthritis
C. Osteoarthritis
D. Pyrophosphate arthropathy
49. Based on this coronal CT of a 58-year-old woman with hip pain, what is the
B. Osteoarthritis
C. Femoroacetabular impingement
D. Subcapital fracture
50. Based on this lateral radiograph of the hand, what is the best diagnosis?
A. Osteoarthritis
B. Pyrophosphate arthropathy
C. Gouty arthritis
D. Rheumatoid arthritis
51. Which percentage most closely approximates the volume of chondrocytes in
articular cartilage?
A. 99%
B. 67%
C. 33%
D. 1%
52. Based on this AP standing radiograph of both knees in a 40-year-old woman,
what is the best diagnosis?
A. Osteoarthritis
C. Pyrophosphate arthropathy
D. Osteoporosis
53. Based on this hand radiograph, what is the best diagnosis?
B. Erosive osteoarthritis
D. Systemic lupus erythematosus
54. Which joints are typically spared in rheumatoid arthritis when it involves the
upper limb?
A. Distal interphalangeal
B. Wrist
C. Elbow
D. Shoulder
55. Based on this radiograph of the wrist, what is the best diagnosis?
A. Scapholunate advanced collapse
B. Scaphoid osteonecrosis
C. Rheumatoid arthritis
D. Systemic lupus erythematosus
56. What is the best diagnosis?
A. Greater tuberosity fracture
B. Rotator cuff tear
C. Calcific tendinosis
57. What is the cardinal feature of pigmented villonodular synovitis on MRI that
allows it to be distinguished from other entities in the differential diagnosis?
A. Rim enhancement following intravenous Gd
B. High signal on both T1 and T2 MRI
C. Low signal on fat-suppressed MRI
D. Blooming on GRE MRI
58. Based on this weight-bearing AP foot radiograph in this woman with chronic
foot pain, what is the best diagnosis?
A. Bunion
B. Hallux rigidus
C. Freiberg infraction
D. Acquired flatfoot
59. Weight-bearing lateral radiograph of the ankle in a 25-year-old woman with
chronic foot pain shows what condition?
A. Tarsal coalition
B. Subtalar arthritis
C. Posttraumatic calcaneal deformity
D. Accessory navicular syndrome
60. Which of the abnormalities associated with the bunion deformity is generally
considered to be the underlying problem that should be corrected if surgery
is to be successful?
A. Valgus alignment of the great toe
B. Varus alignment of the first metatarsal
C. Uncovering of the first metatarsal head
D. Lateral subluxation of the sesamoids
61. What complication of this total hip replacement is shown?
A. Metallosis
B. Osteolysis
C. Infection
D. Fracture
62. What type of knee implant is shown here?
A. Antibiotic-loaded cement spacer
B. Bicondylar total knee replacement
C. Medial unicondylar total knee replacement
D. Knee hemiarthroplasty
63. Which complication or outcome does not occur with metal-on-metal total hip
replacements?
A. Metallosis
B. Polyethylene osteolysis
C. Aseptic lymphocyte-dominated vasculitis-associated lesion
D. Pseudotumor formation
64. What is the best diagnosis regarding the radiographs of this shoulder
prosthesis?
A. Posterior dislocation of anatomic shoulder prosthesis
B. Anterior dislocation of anatomic shoulder prosthesis
C. Posterior dislocation of reverse shoulder prosthesis
D. Anterior dislocation of reverse shoulder prosthesis
65. Joint replacement arthroplasty has been performed at the second through
fifth metacarpophalangeal joints in a patient with underlying rheumatoid
arthritis. The implants have been manufactured from what material?
A. Polyethylene
B. Titanium alloy
C. Silicone
D. Pyrolytic carbon
66. What is the most common indication for radial head replacement?
B. Radiocapitellar osteoarthritis
C. Anterior radial head dislocation
D. Displaced radial head fracture
67. Based on this radiograph, what is the best diagnosis?
A. Paget disease
B. Osteopetrosis
C. Polyostotic fibrous dysplasia
D. Sickle cell disease
68. Based on this radiograph, what is the best diagnosis?
A. Osteoporosis
B. Achondroplasia
D. Thalassemia
69. Which of the following is the most common nonlethal form of dwarfism?
A. Thanatophoric dwarfism
B. Pseudoachondroplasia
C. Morquio syndrome
D. Achondroplasia
70. Based on this detail of a PA radiograph of the hand, what is the best
diagnosis?
A. Sarcoidosis
B. Hyperparathyroidism
C. Erosive osteoarthritis
D. Tophaceous gout
71. Based on this detail of a PA radiograph of the hand, what is the best
diagnosis?
A. Sarcoidosis
C. Erosive osteoarthritis
D. Tophaceous gout
72. According to the U.S. Preventative Services Task Force, which population
should be routinely screened for osteoporosis?
A. Postmenopausal women on hormone replacement therapy
B. Women with obesity (BMI >30)
C. Women who are 65 years or older
D. Men who are 85 years or older
73. MRI of the knee was performed in a 70-year-old man with complaints of
chronic knee pain. What is the most important diagnosis to make from this
coronal T1 MRI?
A. Lateral meniscal tear
B. Lymphoma
C. Paget disease
D. Osteonecrosis
74. What is the best diagnosis in a 70-year-old patient with chronic thigh pain
and history of osteoporosis?
A. Bisphosphonate insufficiency fracture
C. Osteomalacia
D. Osteoid osteoma
75. A patient with type 2 diabetes presents with osteomyelitis of the fifth
metatarsal head. Which of the following is the most likely route of spread for
this infection?
A. Hematogenous spread via arteries
B. Hematogenous spread via veins
C. Lymphatic spread
D. Contiguous spread via skin ulcer
76. What is the best diagnosis on these axial T2 FS (A) and T1 FS (B) Gd MRI
of the calf in a patient with leg swelling?
A. Pyomyositis
B. Sarcoma
C. Mazabraud syndrome
D. Gastrocnemius strain
77. What is the best diagnosis on these AP (A) and lateral (B) radiographs of the
forearm?
A. Insufficiency fracture
B. Chronic osteomyelitis
C. Foreign body reaction
D. Paget disease
78. In acute osteomyelitis, what is the classic MRI pattern of bone marrow signal
abnormality?
A. High T1, high T2, nonenhancing
B. Low T1, high T2, nonenhancing
C. High T1, low T2, enhancing
D. Low T1, high T2, enhancing
79. Based on these coronal T1 (A) and PD FS (B) MRI, what is the best
diagnosis?
A. Enchondromatosis
B. Multiple bone infarcts
C. Marrow reconversion
D. Non-Hodgkin lymphoma
80. Based on this axial CT of the chest, what is the best diagnosis?
A. Thalassemia
B. Hemophilia
C. Sickle cell disease
D. Polycythemia vera
81. Which condition affecting the bone marrow is most closely associated with
osteonecrosis?
A. Hemophilia
B. Thalassemia
C. Sickle cell disease
D. Myelofibrosis
82. The ultrasound transducer has been placed transversely over the anterior
aspect of the left proximal humerus. Which structure is the lesser tuberosity?
A. Structure A
B. Structure B
C. Structure C
D. Structure D
83. A 50-year-old patient presents for ultrasound evaluation of the Achilles

tendon. What is the diagnosis from this longitudinal sonogram of the middle
(A) and distal (B) Achilles tendon?
A. Normal
B. Tendinosis
C. Partial tear (grade 2)
D. Complete tear (grade 3)
84. Anisotropy artifact may resemble which sonographic finding of tendon
injury?
A. Hypoechoic region
B. Tendon thickening
C. Peritendinous fluid
D. Posterior shadowing
85. A 41-year-old man presents for CT-guided core needle biopsy of a left tibial
mass concerning for sarcoma. The mass not only appears to be centered in
the posterior cortex of the proximal tibial metaphysis but also demonstrates
involvement of the adjacent tibialis posterior muscle. The referring surgeon
has requested core needle biopsy of both the intraosseous and intramuscular
components of the suspected sarcoma. Which approach for CT-guided core
needle biopsy will likely minimize the ultimate morbidity to the patient after
surgical resection?
A. Posterior via the posterior compartment
B. Medial via the posterior compartment
C. Lateral via the lateral compartment
D. Anterior via the anterior tibial cortex
E. Lateral via the anterior compartment
86. A patient for shoulder arthrogram is positioned supine on the fluoroscopy

table with the arm externally rotated. A needle is placed via an anterior
approach so that it contacts the upper medial quadrant of the humeral head.
Through which normal structure has the needle likely traversed?
A. Supraspinatus tendon
B. Subscapularis tendon
C. Superior glenohumeral ligament
D. Middle glenohumeral ligament
87. After wrist arthrography with injection into the radiocarpal compartment,
contrast is normally found between which 2 bones?
A. Ulnar head and distal radius
B. Triquetrum and pisiform
C. Scaphoid and lunate
D. Capitate and hamate
88. A young woman presents with foot pain and tenderness in the ball of the foot
after a long hike. Initial radiographs were normal. Her symptoms did not
improve after 2 weeks of rest. Short-axis PD FS MRI through the first
metatarsal head (M1). Which diagnosis is the most strongly supported by the
image?
A. Bunion
B. Sesamoiditis
C. Hallux rigidus
D. Morton neuroma
89. Proximal left thigh pain and mass in a fitness enthusiast. Axial PD FS MRI
of the left thigh. Which diagnosis is best supported by the image?
A. Abscess
B. Soft-tissue sarcoma
C. Myotendinous strain
D. Myositis ossificans
90. Which of the following radiographic features is most characteristic of
osteoarthritis?
A. Fusiform soft-tissue swelling
B. Osteoporosis
C. Erosions
D. Subchondral sclerosis
91. Which radiologic feature best distinguishes osteosarcoma from
osteomyelitis?
A. Metaphyseal location
B. Codman triangle
C. Permeated bone destruction
D. High T2 signal on MRI
92. What surgical procedure is represented by this radiograph of the lower leg?
A. Open reduction and internal fixation
B. Limb-lengthening
C. Bone transport
D. Pin-rod external fixation
93. A 35-year-old man with a swollen thigh. Based on this cross-table lateral
radiograph, what is the best diagnosis?
A. Chondrosarcoma
B. Osteosarcoma
C. Lymphoma
D. Ewing sarcoma
94. A recreational runner with knee pain. Based on this coronal PD FS MRI of
the knee, what is the best diagnosis?
A. Osteosarcoma
B. Osteomyelitis
C. Stress fracture
D. Ewing sarcoma
95. Which of the following elbow ligaments stabilizes the radial head against
posterior subluxation?
A. Lateral ulnar collateral ligament
B. Anterior band of the ulnar collateral ligament
C. Posterior band of the ulnar collateral ligament
D. Transverse band of the ulnar collateral ligament
96. A 35-year-old man with a lump behind his knee. Based on this sagittal CT of
the distal femur, what is the best diagnosis?
A. Periosteal chondroma
B. Osteochondroma
D. Parosteal osteosarcoma
97. Diabetic neuropathic osteoarthropathy of the foot most commonly involves
which joints?
A. Chopart
B. Subtalar
C. Metatarsophalangeal
D. Lisfranc
98. A 58-year-old woman with total knee replacement, but she is unable to walk
on it. Based on the lateral radiograph, which of the following most accurately
describes her knee problem?
A. Tear of the posterior cruciate ligament
B. Anterior dislocation of the knee
C. Polyethylene separation from the tibial tray
D. Particle disease with osteolysis and component loosening
99. A 63-year-old man with shoulder pain. Which of the following is the most
suitable diagnosis?
A. Gunshot wound
B. Surgical neck fracture
C. Pseudotumor
D. Pathologic fracture
100. Which of the following radiologic findings is most typical of a tendon tear?
A. Photopenic on radionuclide bone scan
B. Hypoechoic on ultrasonography
C. Blooming on GRE MRI
D. High attenuation on CT
Answers to Self-assessment Questions

1. D Transverse fracture with butterfly fragment (Chapter 1).
2. C Torsion (Chapter 1).
3. D Open fracture (Chapter 1).
4. B Posterior shoulder dislocation (Chapter 2).
5. B Rotary subluxation of the scaphoid (Chapter 2).
6. C Monteggia (Chapter 2).
7. B Displaced transcervical femoral neck fracture (Chapter 3).
8. D Calcaneal fracture (Chapter 3).
9. A Anterior cruciate ligament tear (Chapter 3).
10. D Remodeling (Chapter 4).
11. A Compression (Chapter 4).
12. C Change in position (Chapter 4).
13. A Lateral meniscus, radial tear (Chapter 5).
14. C Transient lateral patellar dislocation (Chapter 5).
15. B Anterior tibia (Chapter 5).
16. B Supraspinatus (Chapter 6).
17. C Infraspinatus (Chapter 6).
18. A Anterior-superior (Chapter 6).
19. C Medial collateral ligament (Chapter 7).
20. B Posterior fat pad (Chapter 7).
21. A Partial tear of the ulnar collateral ligament (Chapter 7).
22. B Intertrochanteric fracture (Chapter 8).
23. A Anterior labrum (Chapter 8).
24. D Suspected labral tear (Chapter 9).
25. A Scaphoid waist fracture (Chapter 9).
26. C Ulnar impaction syndrome (Chapter 9).
27. D Pisiform (Chapter 9).
28. A Stress fracture (Chapter 10).
29. B Tibialis posterior (Chapter 10).
30. C Flexor hallucis longus (Chapter 10).
31. B Cartilage-forming tumor (Chapter 11).
32. C Sunburst (Chapter 11).
33. A Thin sclerotic margin (Chapter 11).
34. B Osteochondroma (Chapter 12).
35. B Aneurysmal bone cyst (Chapter 12).
36. D Giant cell tumor (Chapter 12).
37. B Osteosarcoma (Chapter 13).
38. A Chondrosarcoma (Chapter 13).
39. D Adamantinoma (Chapter 13).
40. C Metastatic disease (Chapter 14).
41. A Metastatic prostate cancer (Chapter 14).
42. D Foot (Chapter 14).
43. B Loose bodies in a Baker cyst (Chapter 15).
44. C Lipoma (Chapter 15).
45. C Primary soft-tissue sarcomas are more common (Chapter 15).
46. C Psoriatic arthritis (Chapter 16).
47. D Calcium pyrophosphate dihydrate deposition disease (Chapter 16).
48. C Osteoarthritis (Chapter 16).
49. B Osteoarthritis (Chapter 17).
50. A Osteoarthritis (Chapter 17).
51. D 1% (Chapter 17).
52. B Rheumatoid arthritis (Chapter 18).
53. D Systemic lupus erythematosus (Chapter 18).
54. A Distal interphalangeal (Chapter 18).
55. A Scapholunate advanced collapse (Chapter 19).
56. C Calcific tendinosis (Chapter 19).
57. D Blooming on GRE MRI (Chapter 19).
58. D Acquired flatfoot (Chapter 20).
59. A Tarsal coalition (Chapter 20).
60. B Varus alignment of the first metatarsal (Chapter 20).
61. B Osteolysis (Chapter 21).
62. A Antibiotic-loaded cement spacer (Chapter 21).
63. B Polyethylene osteolysis (Chapter 21).
64. D Anterior dislocation of reverse shoulder prosthesis (Chapter 22).
65. C Silicone (Chapter 22).
66. D Displaced radial head fracture (Chapter 22).
67. B Osteopetrosis (Chapter 23).
68. C Osteogenesis imperfecta (Chapter 23).
69. D Achondroplasia (Chapter 23).
70. A Sarcoidosis (Chapter 24).
71. B Hyperparathyroidism (Chapter 24).
72. C Women who are 65 years or older (Chapter 24).
73. C Paget disease (Chapter 25).
74. A Bisphosphonate insufficiency fracture (Chapter 25).
75. D Contiguous spread via skin ulcer (Chapter 25).
76. A Pyomyositis (Chapter 26).
77. B Chronic osteomyelitis (Chapter 26).
78. D Low T1, high T2, enhancing (Chapter 26).
79. B Multiple bone infarcts (Chapter 27).
80. A Thalassemia (Chapter 27).
81. C Sickle cell disease (Chapter 27).
82. C Structure C (Chapter 28). A, greater tuberosity; B, transverse humeral
ligament; C, lesser tuberosity; D, bicipital groove.
83. D Complete tear (grade 3) (Chapter 28).
84. A Hypoechoic region (Chapter 28).
85. D Anterior via the anterior tibial cortex (Chapter 29).
86. C Superior glenohumeral ligament (Chapter 29).
87. B Triquetrum and pisiform (Chapter 29).
88. B Sesamoiditis (Chapter 20).
89. C Myotendinous strain (Chapter 8).
90. D Subchondral sclerosis (Chapter 17).
91. B Codman triangle (Chapter 11).
92. C Bone transport (Chapter 4).
93. B Osteosarcoma (Chapter 13).
94. C Stress fracture (Chapter 1).
95. A Lateral ulnar collateral ligament (Chapter 7).
96. D Parosteal osteosarcoma (Chapter 13).
97. D Lisfranc (Chapter 20).
98. C Polyethylene separation from the tibial tray (Chapter 21).
99. D Pathologic fracture (Chapter 14).
100. B Hypoechoic on ultrasonography (Chapter 28).
INDEX
Note: Page numbers followed by “f” indicate figures and “t” indicate tables.
A
ABC (aneurysmal bone cyst), 216–217, 216f–217f
formation, 208
Abduction, 111
Abduction and external rotation (ABER) position, 107
Abduction stress, UCL, 170
Abductor pollicis longus (ABPL) tendon, 168
Accessory adductor digiti minimi, 168, 168f
Accessory muscles, 264, 274f
Accessory navicular syndrome, 182, 184f, 341–342, 342f
Accessory soleus, 264, 274f
Acellular fibrous stroma, 243
Acetabular fractures, 39–41, 42f–43f
anterior and posterior columns, 40
ilium, 39
ischium, 39
pubis, 39
simple transverse fractures, 41
transverse fracture, 40
T-shaped fracture, 40
Acetabular labral injuries, 153, 159f–160f
Acetabular labral tear, 145
Acetabular labrum, 146, 147f, 316, 319f
Acetabulum pedis, 331
Achilles tendinopathy and partial tear, 178, 178f
Achilles tendinosis, 472, 473f–474f
Achilles tendon, 178, 180
ultrasound evaluation, complete tear, 521f
Achondroplasia, 390–391, 390f–391f, 517f
ACJ. See Acromioclavicular joint (ACJ)
ACL (anterior cruciate ligament) injury
myxoid degeneration, 94, 96f
reconstruction, 94, 95f
tear, 94, 94f
Acquired flatfoot
chronic pain, 513f
medial longitudinal arch, 331
pes planovalgus, 332, 334f
treatment of, 332, 335f
weight-bearing radiograph, 332, 334f
Acrodysostosis, 389, 390f
Acromegaly, 416, 417f
Acromioclavicular joint (ACJ), 31–32, 35f, 114, 116f, 299
buttonholing event, 129
diagnosis and classification, 125
gravity-assisted acromioclavicular displacement, 129
ligamentous lesions, 125, 129t
management of, 129
Rockwood classification, 125, 128f
Rockwood type I, 125, 129f
Rockwood type II, 125, 130f
Rockwood type III, 125, 130f
Rockwood type IV, 129, 131f
Rockwood type V, 129
Rockwood type VI, 129
treatment planning, 125
visualization of, 125
Acute inflammatory synovitis, 317
Adamantinoma, tibia, 234, 240f
Adductor aponeurosis, 171
Adverse local tissue reaction (ALTR), 153
AFIP (Armed Forces Institute of Pathology), 194
Aggressive lesions, 198
Allergy, lidocaine, 479
American Academy of Orthopaedic Surgeons Web site, 371
Amyloid arthropathy, 321, 321f
Anaplastic sarcoma, 227
Anatomic shoulder hemiarthroplasty, 371, 373f
Anatomic variation, anterior-superior, 499f
Anconeus epitrochlearis, 138, 139f
Aneurysmal bone cyst (ABC), 216–217, 216f–217f, 505f
formation, 208
Anisotropy artifact, 460, 461f, 521f
Ankle
dermatomyositis, 302–303, 306f
injection, 483, 487f
injuries
abnormal fluid signal intensity, 181
accessory navicular syndrome, 182, 184f
Achilles tendinopathy and partial tear, 178, 178f
Achilles tendon, 178, 180
acute ankle fractures, 182, 183f
anatomy, 176, 177f
ankle syndesmosis, 180
anterior talofibular ligament (ATFL), 176, 178f
bone bruises, 182, 183f
calcaneofibular ligament, 176
calcaneus fracture, 179, 496f
“chevron sign” deformity, 179
complete tendon tear, 178, 179f
deltoid ligament sprain, 180, 182f
dictation checklist, 176
distal fibular metaphysis, 176
distal tibia, 176
flexor hallucis longus strain, 179, 181f, 503f
fracture fragments, 178
hypertrophied peroneal tubercle, 179
impingement syndromes, 182, 184f
lateral ankle sprains, 180
lateral collateral ligament, 176
linear abnormalities, 182
Lisfranc injury. See Lisfranc injury
longus tendons, 178
medial ankle sprains, 180
medial impingement syndromes, 180
metatarsophalangeal (MTP) joint, 176
navicular and medial cuneiform bones, 178
ossicles/sesamoids injuries, 182
osteochondral lesions, talar dome, 182, 183f
peroneal tendon injuries, longitudinal tear, 179, 180f
peroneus brevis, 178
posterior talofibular ligaments (PTFL), 176, 178f
pseudoarticulation/synchondrosis, 182
screw, 497f
sinus tarsi, 176, 181
stress fractures. See Stress fractures
stress reaction talus, 182, 182f
styloid process, 178
subacute ankle sprain, 180, 181f
superior peroneal retinaculum (SPR), 178
talocalcaneal joints, 176
tarsal coalition, 513f
tarsal tunnel, 176, 178
tibialis anterior tendon injuries, 179, 180f
tibialis posterior tendon injuries, 178, 179f, 503f
turf toe. See Turf toe
mortise
ankle sprains, 52
AO-Weber classification, 49
articular surfaces, 48
axial compression fractures, 52
calcaneofibular ligament, 48
fibular fracture, 50
foot abduction/eversion, 50
foot adduction/inversion, 49
isolated lateral malleolar external rotation injury, 49
lateral malleolus, 48–49
Lauge-Hansen classification, 49
medial malleolus, 48, 49
proximal fracture, 50
talus, 48
tibial and fibular shafts, 48
tillaux fracture, 52
Wagstaffe-Le Fort fracture, 52
surgery and replacement
arthrodesis, 361–362, 364f
aseptic loosening, 363, 367f
designs of, 362
factors, 362
INBONE II prosthesis, 362, 365f
Infinity prosthesis, 362, 366f
Salto-Talaris prosthesis, 362, 365f
STAR prosthesis, 362, 366f
talar osteotomy, 363
syndesmosis, 180
ultrasound, 472–474, 473f–476f
Ankylosing spondylitis, 304, 306
in lumbar spines, 306, 307f
sacroiliitis, 307, 308f
traumatic cervical spine fracture, 308, 308f
Ankylosis, 278
Annular pulley tear, 172, 173f
Anterior and posterior central root ligaments, 83
Anterior cruciate ligament (ACL) injury
myxoid degeneration, 94, 96f
reconstruction, 94, 95f
tear, 94, 94f, 497f
Anterior-inferior glenohumeral joint capsule, 107
Anterior talofibular ligament (ATFL), 176, 178f
Anterolateral impingement, 182
Anterosuperior rotator cuff tears, 125
Antibiotic-impregnated beads, 76
Antiepileptic drug–related bone disease, 422–423, 425f
Apophysis, 211
Arachnodactyly, 395, 395f
Armed Forces Institute of Pathology (AFIP), 194
Arthritis
demographics, 276, 281, 281t
diagnosis of, 276
factors, 276
Occam’s Razor vs. Hickam’s Dictum, 276, 281–282
pattern approach, 276, 278–279, 281f
radiographic hallmarks, 276
ankylosis, 278
arthropathy, 276
cartilage damage, 276
chondrocalcinosis/tophi, 277, 279f
erosions, 277, 279f–280f
forms of, 276, 277t
“hallmark” findings, 277, 277t
joint space narrowing, 276, 278
osteophyte formation, 277, 278f
sclerosis, 278
soft-tissue swelling, 277–278, 280f–281f
subchondral cyst formation, 278
subluxation, 278
reactive, 308–309, 309f
Sutton law
forms of, 276, 277t
rheumatism, 276
“the Big Three” diagnosis, 276, 277t
Arthrocentesis, 485–486, 489
Arthrodesis
ankle surgery, 361–362, 364f
hip surgery, 350, 352, 353f
Arthrography
ankle injection, 483, 487f
bupivacaine, 481
chondrolysis, 481
complications of, 481, 481t
contrast mixture, MR arthrography, 481
elbow injection, 482, 484f
foot injection, 483–484, 488f
gadolinium-based solution, 481
hip injection, 483, 486f
informed consent, 479, 480t
intra-articular pathology, 481
iodine-based contrast medium, 481
knee injection, 483, 487f
shoulder injection, 481–482, 482f–483f
wrist injection, 482–483, 485f
Arthropathy, 276
amyloid, 321, 321f
cuff tear, 326–327, 327f–328f
hydroxyapatite, 316–317, 319f
pyrophosphate
calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, 316,
316f, 318f
of knee, 316, 318f
with scapholunate advanced collapse wrist, 316, 316f
of shoulder, 316, 318f
Arthroplasty
American Academy of Orthopaedic Surgeons Web site, 371
elbow arthroplasty. See Elbow, arthroplasty
hand arthroplasty. See Hand, arthroplasty
hip surgery, 353, 353f
shoulder arthroplasty. See Shoulder, arthroplasty
types, 371
wrist arthroplasty. See Wrist, arthroplasty
Articular cartilage, 146, 277, 280f, 296, 314–315
chondrocytes, 511f
injury
osteochondral injury, 102, 103f
osteochondral loose body, 102, 103f
partial thickness cartilage injury, 102, 102f
traumatic full-thickness cartilage defect, 102, 102f
structure of, 283, 284f
Articulated column biomechanics, 92–94, 94f
Artifacts, 407, 407f
ATFL (anterior talofibular ligament), 176, 178f
Athletic pubalgia, 152–153, 158f
Atlantoaxial subluxation, 300–301, 303f
Attrition tendinopathy, 124–125
Avascular necrosis, 76, 446, 448f. See also Osteonecrosis
Avulsion fractures, 142, 497f
forefoot, 55
midfoot, 54
Avulsion injuries
collateral ligament insertion, 16, 17f
distal phalanx, 16, 17f
tensile failure, 16
Avulsion tearing injury, 117, 119f
Axial spondyloarthritis, 304–305
B
Baastrup disease, 291, 294f
Bacterial sacroiliitis, 433
Baker cyst, 260, 267f, 469, 473f
Barton fractures, 22
Basicervical fractures, 146
Benign bone lesions
aneurysmal bone cyst, 216–217, 216f–217f
bone island (enostosis), 205, 206f
chondroblastoma, 210–212, 216f
chondromyxoid fibroma, 212, 213f
desmoplastic fibroma, 214–215, 215f
enchondroma, 210, 211f–212f
epidermoid inclusion cyst, 218–219
fibrous cortical defect (FCD), 212–213, 214f
fibrous dysplasia, 213–214, 215f
giant cell tumor, 219–220, 219f–220f
intraosseous ganglion, 218
intraosseous lipoma, 215–216, 216f
Langerhans cell histiocytosis (LCH), 220–221, 220f
nonossifying fibroma, 212–213, 214f
osteoblastoma. See Osteoblastoma
osteochondroma (exostosis). See Osteochondroma (exostosis)
osteoid osteoma. See Osteoid osteoma
periosteal chondroma, 210, 212f
unicameral bone cyst (UBC), 217–218, 218f
vascular bone lesions, 219, 219f
Benign lesions, 198
soft-tissue sarcomas
aggressive fibromatosis, 259–260, 267f
elastofibroma, 258, 264f
giant cell tumor, tendon sheath, 258, 265f
hemangioma, 258, 264f
lipomas, 257–258, 261f–263f
peripheral nerve sheath tumors, 258–259, 266f–267f
Biceps brachii muscles, 114, 114f
Biceps tendinosis, 125, 127f
Biceps tendons, 114, 114f, 465, 466f
pathology
anterosuperior rotator cuff tears, 125
attrition tendinopathy, 124–125
biceps tendinosis, 125, 127f
dislocation, 125, 127f
impingement tendinopathy, 124
isolated proximal biceps tendon injuries, 125
partial tears, 125
pulley injuries, 125
spectrum of, 125, 126f
split tear, 125, 127f
tendinopathy with subluxation, 124
tendon rupture, 125, 127f
traumatic/nontraumatic injuries, 125
Bicipital aponeurosis, 142
Bicipitoradial bursa, 137, 137f
Bifid median nerve, 168, 169f
Bilateral brachydactyly, 392, 393f
Bilateral femoral endoprostheses, 354, 354f
Bilateral plexiform neurofibromas, 397, 397f
Biomet Discover prosthesis, 375
Bisphosphonates, 421, 423f
Bizarre parosteal osteochondromatous proliferation (BPOP), 209–210, 211f
Blastic lesions, 249
Blastic metastases, 243, 244f
Bone biomechanics, 1
avulsion fragment, 3, 3f
bone bruises, 4, 5f
compact bone, 2
compressive component, 1
crushing force, 2
deformation, 1–2
ductility, 1
elastic recoil, 1
force, 1–2
fractures, 2–4
loading, 1, 2–4, 2f, 494f
longitudinal compressive loading, 3
oblique fracture, 3, 4f
osteons, 2
penetrating injury, 2
rotational loading, 3
shear component, 1
spiral fracture, 3–4, 4f, 5f
stiffness, 1
tapping injury, 2, 2f
tensile component, 1
tiny avulsion fragment, 3, 3f
traction or tension fractures, 3
transverse fracture, 3, 3f
Bone bruise pattern, anterior tibia, 498f
Bone cement, 250
Bone destruction, 192
permeated, 192, 194f
Bone disorder, 262, 271f–272f
Bone dysplasias, adults
diagnosis
acrodysostosis, 389, 390f
congenital dysplasia, 387
dysplastic appearance, 388, 388f
European Skeletal Dysplasia Network, 389
genetic counseling, 387
gracile bones and peculiar soft tissues, 388, 389f
Hallermann-Streiff syndrome, 387
hand-foot-uterus syndrome, 388
International Skeletal Dysplasia Registry, 389
National Organization for Rare Diseases, 390
neuromuscular diseases, 388
NIH Office of Rare Disease Research, 390
Online Mendelian Inheritance in Man (OMIM) site, 389
paraplegia/quadriplegia, 388
PubMed search, 389
size discrepancy, ribs and ilium, 388, 388f
radiology
achondroplasia, 390–391, 390f–391f
dactyly, 391–392, 392f–394f
enchondromatosis, 393, 394f–395f
madelung deformity, 401–402, 402f
Marfan Syndrome, 393, 395, 395f
melorheostosis, 401, 401f
multiple hereditary exostoses, 395–396, 396f–397f
neurofibromatosis, 397, 397f–398f
osteogenesis imperfecta, 397–398, 398f–399f
osteopathia striata, 400–401, 401f
osteopetrosis, 398–400, 399f–400f
osteopoikilosis, 400, 400f
pseudoachondroplasia, 391, 391f
Bone grafts, 73, 74f
implants, 73–74
Bone island (enostosis), 205, 206f, 249, 249f
Bone marrow conditions
bone marrow edema syndrome, 449–450, 452, 453f
hemophilia, 453–454, 455f–456f
lysosomal storage disorders, 456, 457f–458f
myelofibrosis, 454–456, 456f–457f
myeloid cells, 444
osteonecrosis. See Osteonecrosis
red marrow reconversion, 444, 445f
sickle cell disease, 452, 454f
signal characteristics, 444
thalassemia, 452–453, 454f
yellow marrow reconversion, 444, 445f
Bone marrow edema syndrome, 449–450, 452, 453f
Bone mineral densitometry, 405–407, 406f–407f, 406t, 408t
Bone proliferation, 192
Bone-tendon-bone autograft, 94
Bone transport, 524f
Bone tumors
incidence, 192
lesion location, 192
longitudinal locations, 192, 193t
transverse locations, 192, 193t
metastatic osteosarcoma, 199, 201f–202f
musculoskeletal lesions, 192
patient factors, 192
primary malignant bone tumors, types, 192, 193t
rate of growth/aggressiveness
Armed Forces Institute of Pathology (AFIP), 194
bone destruction, 192
bone proliferation, 192
Codman triangle, 194, 195f
cortical penetration, 193, 195, 195f
cortical shell, 193, 195f
grading system, 194, 196t
higher-grade growth rates, 195
lower-grade growth rates, 195
moth-eaten bone destruction, 192, 194f
with no sclerotic margin, 194, 196f
periosteal reaction layers, 193, 195f
permeated bone destruction, 192, 194f
in proximal femur, 192, 193f
sclerotic rim, 193, 195f
sunburst periosteal reaction, 194, 196f
solitary bone lesion, 202, 202f–203f
staging
active lesions, 198
aggressive lesions, 198
AJCC prognostic stage groups, 199, 199t
benign lesions, 198
latent lesions, 198
lung metastases, chest CT, 198
malignant lesions, 198–199
Musculoskeletal Tumor Society, 198–199
osteosarcoma, elderly patient, 198, 199f
tissue characterization, 192
chondroid matrix, 197
fibrous matrix, 197, 199f
flocculent cartilage matrix mineralization, 197, 198f
intermediate (ground-glass) mineralization, 197, 199f
matrix mineralization, 195, 197, 197t
myxoid matrix, 197
osteoid matrix, 197, 197f
punctate cartilage matrix mineralization, 197, 198f
rings-and-arcs cartilage matrix mineralization, 197, 198f
treatment
bone/cement grafting, 199
Ewing sarcoma, 199, 200f
metal artifact reduction algorithm, 199
neoadjuvant and adjuvant therapies, 199
recurrent parosteal osteosarcoma, 199, 201f
recurrent soft-tissue sarcoma, 199, 201f
soft-tissue sarcoma, 199, 200f
“Bony” Bankart, 117–118
Boutonniere injury, 173, 174f
BPOP (Bizarre parosteal osteochondromatous proliferation), 209–210, 211f
Brachialis tendons, 465, 466f
Breast carcinoma
blastic metastases, 243, 244f
lumbar spine, pelvis, and femurs, 245, 246f
lytic metastases, 243, 244f
PET/CT, 243, 245f
spine metastases, 245, 247f
Brodie abscess, 431, 433f
Brown tumor, 409, 410f
healing, 409, 411f
proximal femur, 409, 411f
Bucket handle meniscal tear, 88, 89f
Buford complex, 109, 112f
Bunion deformity, 342, 344f–345f
varus alignment, first metatarsal, 514f
Bupivacaine, 481
Burns/blast injuries, 11f
fireworks, 10–11
high-order explosives, 10–11
osteoporosis, 10
periarticular osseous, 10
secondary blast injuries, 10–11
Bursae, 114, 136–137, 137f
Bursitis, 260–261, 268f
C
Calcaneocuboid joints, 332
Calcaneofibular ligament, 176
Calcaneus, 496f
Böhler’s angle, 54
extra-articular calcaneal fractures, 54
intra-articular calcaneal fractures, 53, 54
stress fractures, 54, 179
sustentaculum tali, 53
Calcific bursitis, 123
Calcific myonecrosis, 262, 271f
Calcific retrocalcaneal bursitis, 316, 319f
Calcific tendinosis, 122, 124f, 512f
Calcified marrow infarcts, 449, 452f
Calcium hydroxyapatite, 302, 305f
Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, 277
acute synovitis, 316
chondrocalcinosis, 315–316
clinical syndromes, 315, 315t
of hand, 316, 317f
pyrophosphate arthropathy, 316, 316f, 318f
Cancellous metaphyseal bone, 242
Capitellar and trochlear fossae, 135
Capitellar epiphysis, 139
Carpal arthrodesis, 377, 380f
Carpal boss, 168, 168f
Carpal instability, 25f
distal radius fractures, 22
dorsal intercalated segment instability, 22
dorsiflexion instability, 22
volar flexion instability, 22
volar intercalated segment instability, 22
wrist sprains, 22
Carpal osseous anatomy, 163, 164f
Carpal tunnel syndrome, 164, 166, 167f , 174
Carpometacarpal (CMC) arthroplasty, 382, 382f–383f, 510f
Cartilage damage, 276
Cartilage-forming tumor, 503f
Catastrophic knee injury, 99, 99f–100f
Cellulitis and subcutaneous abscess, 437–438, 439f
Cement grafting, 199
Charcot joint, 314, 315f
Chauffeur’s fractures, 23
“Chevron sign” deformity, 179
CHL (coracohumeral ligament), 114
Chondroblastoma, 210–212, 216f
Chondrocalcinosis, 277, 279f, 315–316, 409–410
Chondrocytes, 208
Chondroid matrix, 197, 210
Chondrolysis, 481
Chondromyxoid fibroma, 212, 213f
Chondrosarcoma, 210, 225, 231f, 232f
Chopart joint, 331
Chordoma, 233–234, 239f
Chronic kidney disease
periarticular calcinosis, hemodialysis, 262, 272f
in skin and subcutaneous tissues, 262, 271f
Chronic stenosing tenosynovitis, 173
Circumferential bundles, 83
Circumferential collagen bundles, 89
Circumferential/vertical tears, 88, 88f
Clavicle
coracoclavicular (CC) ligaments, 31, 35f
distal clavicle fracture, 31, 35f
Clinodactyly, 391, 392f
Clostridial myonecrosis, 439–440, 441f
Clubfoot (talipes equinovarus), 336
CMC (carpometacarpal arthroplasty), 382, 382f–383f
Codman triangle, 194, 195f
Codman tumor, 210–212, 216f
Cold injuries, 345, 347, 348f
Collagen bundles, 83
Collateral ligaments, 164, 166f
injuries, 170
Colon carcinoma, 245, 247f
Compression fractures, 249
Compressive injuries, 92–93
Congenital dysplasia, 387
Connective tissue disease
dermatomyositis and polymyositis, 302–304, 306f
overlap syndromes, 304
scleroderma, 302, 305f
systemic lupus erythematosus (SLE), 301–302, 305f
Coonrad-Morrey prosthesis, 374, 377f
Coracoclavicular bursa, 114
Coracoclavicular ligament, 114
Coracohumeral ligament (CHL), 114
Coracoid process, 114
Cortical bone, 2, 404
Cortical metastasis, 245, 248f
Corticosteroids, 481
CPPD (calcium pyrophosphate dihydrate crystal deposition disease), 277
acute synovitis, 316
clinical syndromes, 315, 315t
of hand, 316, 317f
pyrophosphate arthropathy, 316, 316f, 318f
Cruciate ligaments, 81–82, 82f
Crystal-associated diseases
articular cartilage, 314–315
biophysical and biochemical interactions, 315
calcium pyrophosphate dihydrate (CPPD) crystal deposition disease. See
Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease
clearance of, 314
crystal deposition, 315, 315t
gout, 317–319
hydroxyapatite deposition disease
acetabular labrum, 316, 319f
calcifications, 316
calcific retrocalcaneal bursitis, 316, 319f
hydroxyapatite arthropathy, 316–317, 319f
ion contaminants, 316
renal failure and hyperparathyroidism, 316–317
subscapularis tendon, 316, 318f
supraspinatus tendon, 316, 318f
Crystal deposition disease, 123
Crystalline arthropathies, 277
Cubital bursitis, 260–261, 268f
Cubital tunnel retinaculum, 143, 143f
Cuff tear arthropathy, 326–327, 327f–328f
Curettage, bone chips, 363–364, 367f
Cushing syndrome. See Hypercortisolism
Cysticercosis, 440, 441f
D
Dactyly, 391–392, 392f–394f
DECT (dual-energy CT), 319, 320f
Degenerative disk disease, 243
Degenerative joint disease, 276
Degenerative spine conditions
ankylosing spondylitis, 290, 293f
annulus fibrosus, 288
degenerative disk disease, 289
degenerative lumbar disk herniation, 289, 292f
diffuse idiopathic skeletal hyperostosis (DISH), 290, 293f–294f
intervertebral disk joints, 287–288, 291f
lumbar degenerative disk disease, 289, 292f
spondyloarthropathies, 290
spondylosis deformans, 289, 292f
Delayed union, 74
Denervation atrophy, infraspinatus, 499f
de Quervain syndrome, 172, 173f, 466, 468f
Dermatomyositis, 302–303, 306f
Desmoplastic fibroma, 214–215, 215f
Destructive lesions, 249
Diabetes mellitus, 416, 417f
Diabetic foot
chronic ulceration and infection, 332
glomerular filtration rate, 333
interdigital arterial calcifications, 332, 334f
neuropathic osteoarthropathy, 332–333, 336f–337f
osteomyelitis, 333
surgical reconstruction, 333, 337f
Diabetic myopathy, 264, 273f
Diabetic neuropathic osteoarthropathy, 525f
Diabetic peripheral neuropathy, 314
Diaphyseal aclasis, 208
Diarthrodial joint
erosions, 277, 279f–280f
marginal osteophyte, 277, 278f
Diffuse blastic metastases, 243, 245f
Diffuse idiopathic skeletal hyperostosis (DISH), 290, 293f–294f
Diffuse large B-cell lymphoma, 228, 235f
Digital extensor mechanism, 210
Discoid lateral meniscus, 92, 93f
with tear, 92, 93f
Disease-modifying antirheumatic drugs (DMARDs), 297
Distal biceps tendon tear, 142, 142f, 465, 466f
Distal fibular metaphysis, 176
Distal interphalangeal (DIP) joints, 164
erosions, 302
Distal radioulnar joint (DRUJ), 163, 377–378, 381f
Distal radius, 22
avulsion fractures, 23
Barton fractures, 22
chronic dislocation, 24
Colles fracture, 22, 26f
distal radioulnar joint subluxation, 24, 27f
forearm. See Forearm
Hutchinson fractures, 23
intra-articular fractures, 22, 26f, 27f
older women, 22
posttraumatic wrist disability, 24
radial styloid, 23
residual/posttraumatic dorsal tilt, 22
TFCC, 22, 23
transverse radial metaphyseal fracture, 22, 26f
ulnar styloid, 23
Distal triceps tendon tear, 143, 143f
Doppler ultrasonography, 369
Dorsal extrinsic ligaments, 164
Dorsal intercalated segment instability, 169
DRUJ (distal radioulnar joint), 163, 377–378, 381f
Dual-energy CT (DECT), 319, 320f
Dual-energy X-ray absorptiometry (DXA), 405–407, 406f–407f
Dwarfism, 390
Dynamic stabilizers, 108
rotator cuff muscles, 111
Dysplasia epiphysealis hemimelica, 208
E
ECRB (extensor carpi radialis brevis), 136
ECU (extensor carpi ulnaris), 163, 173, 173f
tendinosis, 466, 467f
tendon dislocation, 466, 467f
Elastofibroma, 258, 264f
Elbow
arthroplasty
Biomet Discover prosthesis, 375
bipolar radial head replacement, 373, 376f
complications, 373
Coonrad-Morrey prosthesis, 374, 377f
distal humeral yoke, 375
humeral and ulnar components, 374, 376f
indication for, 373
infected total elbow arthroplasty, 375, 378f
linked total elbow arthroplasty, 375, 377f
radial head replacements, 373
radiocapitellar elbow arthroplasty, 375, 379f
total elbow replacement disassembly, 375, 378f
unipolar radial head replacement, 373, 375f
capitellum, 27
coronoid process, 28, 29f
injuries
anconeus epitrochlearis, 138, 139f
annular ligament, 135, 136f
annular recess, 134–135, 136f
anterior humeral recess, 134
articular capsule, 134
biceps brachii and brachialis, 136
bicipital aponeurosis, 142
brachialis muscle, 134
bursae, 136–137, 137f
capitellar and trochlear fossae, 135
capitellar epiphysis, 139
capitellum, pseudodefect, 137, 138f
chronic overuse pattern, 141
circumferential elbow coil, 134
collateral ligament complexes, 135
compression neuropathy, 137
distal biceps tendon tear, 142, 142f
distal triceps tendon tear, 143, 143f
fat pad sign, 135, 135f
flexion and extension, 135
flexor muscles, 136
fluid-sensitive sequences, 139
lateral epicondylitis (tennis elbow), 140, 142f
lateral muscle group, 136
lateral ulnar collateral ligament (LUCL), 135, 136f, 525f
ligament injury, 139–140, 141f
loose body formation, 139
medial apophysitis, 138, 140f
medial epicondylitis (Golfer’s elbow), 140–141, 142f
medial muscle group, 136
muscles of, 135
nerve entrapment, 143–144, 143f–144f
olecranon recess, 134
olecranon stress, 137, 139, 141f
osteochondral disease (OCD), 139, 140f
osteochondral lesions, 137
Panner disease, 139
phased array coil, 134
plica syndrome, 138
posterior muscle group, 136
posterolateral rotatory instability, 135
pronation and supination, 135
radial collateral ligament (RCL) recess, 134
radiohumeral and radioulnar articulations, 134
supracondylar process, 137, 138f
synovial folds/plicae, 138, 139f
trochlear notch, 137
trochoginglymoid joint, 134
ulnar collateral ligament (UCL) recess, 134–135, 135f, 500f
ulna, trochlear ridge, 137, 138f
ulnohumeral articulation, 134
valgus stress, 138
varus stress, 134
intercondylar fractures, 28, 30f
intra-articular olecranon process, 27–28, 29f
posterior elbow fracture-dislocation, 28, 30f
radial head fractures, 27, 28f
radial neck fractures, 27, 29f
synovial chondromatosis, 322, 323f
synovial hypertrophy, 299
ultrasound, 463–465, 466f
Enchondroma, 210, 211f–212f
Enchondromatosis, 393, 394f–395f
Endochondral ossification, 208
Enteropathic spondyloarthropathy, 311, 311f
Entheses, 277, 278f
Enthesophytes, 277, 278t
Epidermoid inclusion cyst, 218–219
Epinephrine, 481
Epiphysis, 211
EPL (extensor pollicis longus) tendon rupture, 466, 468f
Erosions, 277, 279f–280f
articular cartilage, 277, 280f
crystalline deposits/infection, 277
gouty erosion, 277, 280f
with juvenile chronic arthritis, 277, 280f
pannus, 277
periarticular bare areas, 277, 279f
rheumatoid arthritis (RA), 277
metatarsophalangeal and toe joints, 277, 279f
synovial hypertrophy, 277
tophi, 277
Essex-Lopresti fracture, 25, 28f
European Skeletal Dysplasia Network, 389
Ewing sarcoma, 199, 200f
of distal humerus, 230, 237f
femoral shaft, 230, 238f
of lower extremities, 229
of rib, 230, 238f
Exostotic (peripheral) chondrosarcomas, 226, 233f
Extensor carpi radialis brevis (ECRB), 136
Extensor carpi ulnaris (ECU), 136, 163, 173, 173f
tendon dislocation, 466, 467f
Extensor digiti minimi, 136
Extensor digitorum, 136
Extensor hood mechanism, 172
Extensor mechanism injury, 83
Jumper’s knee, 99, 100f
patellar tendon tear, 101, 101f
quadriceps tendon tears, 101, 101f
Extensor pollicis longus (EPL) tendon rupture, 466, 468f
Extensor tendons, 164, 167f
External fixation, 76
bone fragment, 73, 74f
nonunion ilizarov external fixator, 73, 73f
pin fixators, 72, 73f
ring fixators, 73, 73f
Extracapsular fractures, 147
Extrinsic ligaments, 164, 166f
F
FAI. See Femoroacetabular impingement (FAI)
Fat-containing/mineralized lesions, 255
Fat embolism, 75
Fat pad edema, 104, 105f
Fat pad sign, 135, 135f
FCD (fibrous cortical defect), 212–213, 214f
Femoral head
alcoholism and systemic corticosteroids, 444
avascular necrosis, 446, 448f
clinical conditions, 444, 446t
with crescent sign, 445, 447f
with marrow edema, 445, 448f
predominant blood supply, 444
sclerosis, 445, 446f
with subchondral collapse, 445, 447f
with subchondral fracture, 446, 449f
weight-bearing surface, 445
Femoral neck fractures, 146
Femoral neck stress fractures, 148, 150f
Femoral shaft metastasis, 245, 248f
Femoroacetabular impingement (FAI), 153, 160f
acetabular labral pathology, 323
cam- and pincer-type FAI, 323, 326f
crossover sign, 323, 325f
femoral head-neck junction, 323, 325f
os acetabula, 323, 325f
synovial herniation pit, 323, 325f
Femur fracture, 359, 363f
Fibrocartilage menisci, 277, 279f
Fibrocartilaginous structure, 164
Fibromatosis, aggressive, 259–260, 267f
Fibro-osseous tunnel, 166
Fibrous cortical defect (FCD), 212–213, 214f
Fibrous dysplasia, 197, 199f, 213–214, 215f
Fibrous matrix, 197, 199f
Fingers
avulsion injuries, 16
baseball finger, 16
boxer’s fracture, 17, 18f
distal interphalangeal (DIP), 16
distal phalanges, 17, 18f
ligament tear, 16
mallet finger, 16, 17f
metacarpal fracture, 16–17, 18f
phalangeal fractures, 16
phalangeal tuft fractures, 17
proximal interphalangeal (PIP), 16, 18f
skeletal injuries, 16
tendon tear, 16
Flatfoot (pes planus alignment), 331
Flexor tendons, 164, 166, 167f, 172
Flocculent cartilage matrix mineralization, 197, 198f
Fluid-sensitive fat-suppressed sequences, 81
Fluid-sensitive sequences, 172
Fluorescent antinuclear antibody test, 301
Fluoroquinolone-associated tendinopathy, 422, 424f
Foot conditions, nontraumatic, 332f
accessory navicular syndrome, 341–342, 342f
acetabulum pedis, 331
acquired flatfoot
pes planovalgus, 332, 334f
treatment of, 332, 335f
weight-bearing radiograph, 332, 334f
anteroposterior (AP) radiographs, 331
bunion deformity, 342, 344f–345f
Chopart joint, 331
chronic pain, 513f
cold injuries, 345, 347, 348f
corrected clubfoot, 336–337
diabetic foot
chronic ulceration and infection, 332
glomerular filtration rate, 333
interdigital arterial calcifications, 332, 334f
neuropathic osteoarthropathy, 332–333, 336f–337f
osteomyelitis, 333
surgical reconstruction, 333, 337f
diabetic neuropathic osteoarthropathy, 525f
forefoot, 331
Freiberg disease, 343, 346f
Haglund deformity, 338–339, 339f
hallux rigidus, 343, 345f
heel fat pad syndrome, 340, 340f
hindfoot, 331
injection, 483–484, 488f
injuries. See Ankle, injuries
lateral foot alignment, 331, 333f
lateral foot radiographs, 331
lateral longitudinal arch, 331
lesser toe deformities, 345, 347f
Lisfranc joint, 331
medial column, 331
metastases, 508f
midfoot, 331
Morton neuroma, 345, 346f
motion and alignment, 331
plantar aponeurosis, 339
plantar fasciitis, 339, 339f
polydactyly, 391, 392f
psoriatic arthritis, 309, 310f
rheumatoid arthritis (RA), 299–300, 303f–304f
sesamoiditis, 342, 343f, 523f
sinus tarsi syndrome, 340–341, 340f
subtalar joint, 331
talar dome osteochondral defect, 341, 341f
tarsal coalition, 337–338, 338f
tibialis posterior tendon, 331
ultrasound, 474, 477f
Forearm
chronic osteomyelitis, 519f
Essex-Lopresti fracture, 25, 28f
Galeazzi fracture-dislocation, 25, 27f
Monteggia fracture, 25, 27, 28f
radial shaft fracture, 25
radius, 25
tapping fracture, 25
ulnar shaft fracture, 25, 27
Forefoot, 331
dislocation, 54
extra-articular transverse fracture, 55
Jones fracture, 55
stress fracture, 502f
stubbed toe injuries, 56
T-shaped/Y-shaped fractures, 56
Fractures, 20
alignment, 13–14
angulation, 13–14
anterior cruciate ligament tear, 497f
avulsion fractures, 4, 14–15
cartilage injuries, 14, 14f
classification, 15
comminuted fractures, 13
compression fractures, 4
cortical bone fractures, 4
displacement and distraction, 14
distal radius, 22
edema and hemorrhage, 4–5
epidemiology, 1
gunshot wound, 495f
hamate fractures, 21, 21f
healing
acute regional osteoporosis, 62, 63f
bone grafts, 73, 74f
bone resorption, 62
cancellous bone, 64f
closed fracture treatment, 62–63
complications, 75–78, 76t, 77f–79f
dynamic compression, 63
external fixation. See External fixation
external periosteal callus, 62
failure, 73–75, 75f–76f
fiberglass casts, 62, 65f
fibrous tissue, 62
fracture callus, 63
imaging, 78–79
internal fixation, 63
intramedullary (IM) callus, 62
intramedullary rods. See Intramedullary rods
ligament and tendon injuries, 62
muscle activity, 62
open reduction, 63
ossification, 62
plaster casts, 62, 64f
plates. See Plates
primary fracture healing, 63
primary/soft callus, 62
remodeling humeral shaft fracture, 62, 64f
screws. See Screws
secondary fracture healing, 62, 63, 63f
skeletal traction, 63, 65f
soft-tissue healing. See Soft-tissue healing
stable fractures, 62
static compression, 63
transverse fracture, 66f
wires and cables. See Wires and cables
imaging, 4–5
intra-articular fractures, 14
lower extremity fractures. See Lower extremity fractures
lunate fractures, 21
luxation, 14
Monteggia, apex posterior fracture, 496f
MRI, 4–5
osteochondral fractures, 14, 14f
pisiform fractures, 21
position, 14
radial head replacement, 516f
radionuclide bone scans, 5
remodeling, 497f
scaphoid, 20
segmental tibial shaft fractures, 47
shortening and subluxation, 14
spiral, 47
stress, 38
Tc-99m radionuclide bone, 4
transverse tibial shaft fractures, 47
triquetral fractures, 21, 21f
vertical/transverse fractures, 21
waist, 20, 20f
Fragments distraction, 74
Fragments/excessive motion, 75
Freiberg disease, 343, 346f
Frostbite, 345, 347, 348f
Fungal infections, 436, 438
Fusiform soft-tissue swelling, 297, 301, 317
G
Gadolinium, 297
Galeazzi fracture-dislocation, 25, 27f
Ganglion cyst, 260, 267f
Gas gangrene, 439–440, 441f
Gaucher disease, 456, 457f
Giant cell tumor, 219–220, 219f–220f, 505f
tendon sheath, 258, 265f
Glenohumeral instability
ABER position, 117
anterior shoulder dislocation, 116–117
Bankart fracture, 117, 120f
Bankart labral tear (BT), 117–118, 119f
fracture fragment, 117
Hill-Sachs (HS) fracture, 118, 120f
humeral head movement, 117
posterior glenohumeral joint dislocation injuries, 118
recurrent microtrauma, 116
soft-tissue Bankart lesions, 117–118
traumatic glenoid defect/glenoid bone loss, 117
traumatic shoulder instability, 117
Glenohumeral joint. See also Shoulder, injuries
dislocations
anterior shoulder dislocation, 31, 33f
Hill-Sachs lesion, 31, 34f
posterior shoulder dislocation, 31, 34f
Glenoid articular surface, 108
Glenoid fossa, 108
Glenoid labrum, 108, 109f
Gluteus medius, 151, 154f
Gonococcal arthritis, 433
Gout, 317–319
Gouty erosion, 277, 280f
Gouty tophi, 277
Grading system, 194, 196t
Gunshot wounds, 495f
bullet, 9
contaminated material, 9
high-velocity gunshot wounds, 9–10, 10f
jacketed/unjacketed ammunition, 9
low-velocity gunshot wounds, 9
multiple projectiles, 10
plastic and rubber bullets, 10
temporary vacuum cavity, 9–10
vascular and neural structures, 9–10
Guyon’s canal syndrome, 166, 174
H
HAART (highly active antiretroviral therapy), 423
Haglund deformity, 338–339, 339f
Hallermann-Streiff syndrome, 387
Hallux rigidus, 343, 345f, 479, 480f
Hamate fractures, 169, 170f
Hammertoes, 345, 347f
Hamstring muscles, 150, 152f
avulsion of, 151, 152f
Hamstring tendinosis, 469, 472f
Hand
arthritis distribution, 279, 281f
arthroplasty
carpometacarpal (CMC) arthroplasty, 382, 382f–383f
end-stage arthropathy, 382
metacarpophalangeal joints, 382
pyrolytic carbon proximal interphalangeal (PIP) arthroplasty, 382, 385f
silicone metacarpophalangeal (MCP) arthroplasty, 382, 384f
silicone proximal interphalangeal (PIP) arthroplasty, 382, 384f
triscaphe joint, 382
calcium pyrophosphate dihydrate (CPPD) crystal deposition disease of, 316,
317f
and finger ultrasound, 467–468, 470f–471f
inflammatory (erosive) osteoarthritis, 287, 291f
injuries. See Wrist, injuries
osteoarthritis, 510f
rheumatoid arthritis (RA), 297, 299f
sarcoidosis, 517f
systemic lupus erythematosus (SLE), 511f
Hand-foot-uterus syndrome, 388
Handlebar palsy, 174
Hardware loosening, 497f
Healing process, 250
Heel fat pad syndrome, 340, 340f
Hemangioma, 219, 219f, 258, 264f
Hematoma, 261–262, 269f
formation, 150
ultrasound, 460
Hemodialysis, periarticular calcinosis, 262, 272f
Hemophilia, 453–454, 455f–456f
Hereditary multiple exostoses, 208, 208f
Highly active antiretroviral therapy (HAART), 423
Hindfoot, 331
Hip
anterior labrum, labral tear, 501f
chondrosarcoma, 506f
dislocation, 41–42, 44f, 45f
anterior dislocations, 41
posterior dislocations, 41
sciatic nerve injury, 41
dual-energy X-ray absorptiometry (DXA), 405–407, 406f
effusion, 468, 471f
injuries
acetabular labral injuries, 153, 159f–160f
acetabular labral tear, 145
anterior muscles, 146
articular cartilage, 146
athletic pubalgia, 152–153, 158f
basicervical fractures, 146
clinical evaluation, 145
complete tendon tears, 150
elderly patients, 145
extracapsular fractures, 147
femoral neck fractures, 146
femoral neck stress fractures, 148, 150f
femoral nerve, 146, 148f
femoroacetabular impingement (FAI), 153, 160f
gluteus medius, 151, 154f
hamstring muscles, 150–151, 152f
hematoma formation, 150
iliopsoas bursitis, 155, 161f
iliopsoas muscle, 146
intertrochanteric fractures, 147, 149f
intracapsular fractures, 146–147
ischiofemoral impingement, 154, 161f
luteus maximus, 146
medial muscles, 146
multiple muscle groups, 146, 146f
muscle strains and tendon injuries, 150
obturator nerves, 146, 148f
occult hip fractures, 147
osteonecrosis, 148, 151f
partial tendon tears, 150
peroneal nerve, 146
piriformis syndrome, 155
postarthroplasty hip, 153–154, 161f
posterior muscles, 146
proximal femur fractures, 146
psoas muscle, 146
quadratus femoris muscle, 154–155
rectus femoris muscle, 152, 155f
rectus femoris strain, 152, 156f–157f
sciatic nerve, 146, 147f
stress fractures, 147, 153, 149f–151f, 158f
sublabral recess, 146, 147f
subtrochanteric fractures, 147
symptoms, 145
torn muscle fibers, 150
transcervical fractures, 146
transient bone marrow edema syndrome, 149, 151f
trochanteric bursa, 151
trochanteric pain syndrome, 151, 153f
trochanters, 145
intertrochanteric fracture, 67
metastatic prostate cancer, 507f
osteoarthritis, 285, 288f, 510f
osteoporosis, 404, 405f
rheumatoid arthritis (RA), 299, 303f
ultrasound, 468–469, 471f–472f
acetabular cup dislocation, 354, 356f
arthrodesis, 350, 352, 353f
arthroplasty, 353, 353f
aseptic lymphocytic vasculitis–associated lesions, 356, 357f
bilateral femoral endoprostheses, 354, 354f
complications of, 354, 355t
core decompression, 350, 353f
dislocated total hip replacement, 354, 356f
heterotopic ossification, 354, 356f
joint replacement materials, 353–354
loose cemented total hip replacement, 355, 357f
osteolysis, 354–355, 357f
osteotomy, 350, 351f–352f
periprosthetic soft-tissue lesions, 356
polyethylene acetabular liner, 356
radionuclide bone scan, bilateral total hip replacements, 356, 357f
resurfacing hemiarthroplasty, 354, 354f
total hip replacements (THRs), 354, 355f
types, 354
suspected labral tear, 501f
transcervical femoral neck fracture, 496f
HIV infection and AIDS, 441–442
Hodgkin lymphoma, 228–229, 236f
Hoffa disease, 104, 105f
Hoffa fat pad, 85
Humeral head articular surface, 108
Humeral head pseudolesion, 202, 202f–203f
Humerus
anatomic neck fractures, 29
avulsion fracture, 30, 33f
greater tuberosity fractures, 30, 32f
proximal fragment, 29
surgical neck fracture, 29, 31f
Humphrey ligament, 83
Hyaline articular cartilage, 87, 114, 277, 279f
Hydroxyapatite arthropathy, 316–317, 319f
Hydroxyapatite deposition disease
calcifications, 316
calcific retrocalcaneal bursitis, 316, 319f
hydroxyapatite arthropathy, 316–317, 319f
ion contaminants, 316
renal failure and hyperparathyroidism, 316–317
Hypercortisolism
muscle wasting, 416
nonendocrine adrenocorticotropic hormone–producing tumors, 415
osteonecrosis, 415–416
Hyperparathyroidism, 517f
autonomous parathyroid function, 409
brown tumor, 409, 410f
healing, 409, 411f
proximal femur, 409, 411f
osteoclastic bone resorption, 409
primary hyperparathyroidism, 409
sacroiliac joint bone resorption, 409, 409f
secondary hyperparathyroidism, 409–410, 410f–411f
osteosclerosis, 409, 411f
Hypertrophic osteoarthritis, 479, 480f
Hypertrophic osteoarthropathy, 424, 426f
Hyperuricemia, 317, 319
Hypervascular renal cell carcinoma metastasis, 243, 243f
Hypervitaminosis D, 419–420, 420f
Hypoechoic abnormality, 460
I
Idiopathic tumoral calcinosis, 262–263, 272f
Iliopsoas bursitis, 155, 161f
Iliopsoas muscle, 146
Iliotibial (IT) band syndrome, 104, 104f
Implanted metal components, 353–354
INBONE II prosthesis, 362, 365f
Inclusion body myositis, 263–264, 273f
Inferior glenohumeral ligament, 108, 110f
Infinity prosthesis, 362, 366f
Inflammatory arthritis
connective tissue disease. See Connective tissue disease
Juvenile idiopathic arthritis, 311, 312f–313f
rheumatoid arthritis (RA). See Rheumatoid arthritis (RA)
spondyloarthritis (spondyloarthropathy). See Spondyloarthritis
(spondyloarthropathy)
Inflammatory disease, 277
Inflammatory myopathy, 263–264, 273f
Inflammatory myositis, 303, 306f
Inflammatory periostitis, 309, 310f
Infrapatellar tendinosis, 472, 473f
Infraspinatus muscle, 109
Intercondylar-stabilized total knee replacement, 359, 361f
Interdigitating erosions, 309, 309f
Intermediate (ground-glass) mineralization, 197, 199f
Intermeniscal ligaments, 83, 86f
International Skeletal Dysplasia Registry, 389
Interosseous bursae, 137
Intersection syndrome, 172
Intertrochanteric fractures, 43, 46f, 147, 149f, 501f
degree of displacement, 43
femoral shaft affect, 43
isolated fractures, 43
Intra-articular injections, 479, 480f
Intracapsular fractures, 42–43, 45f, 46f, 74, 146–147
displaced fractures, 42
femoral neck fractures, 42
nondisplaced fractures, 42
subcapital femoral neck fractures, 42
Intramedullary rods
closed nailing, 71
distal locking screws, 72f
dynamization, 72
endosteal blood supply, 72
gamma nail, 72, 72f
long-bone fractures, 71
open nailing, 71
periosteal blood supply, 72
proximal locking screws, 72f
subtrochanteric femur fractures, 72, 72f
Intramuscular hemangioma, 258, 264f
Intraosseous ganglion, 218
Intraosseous lipoma, 215–216, 216f
Intrinsic carpal ligaments, 164
Intrinsic ligament injury, 170, 171f
Ischiofemoral impingement, 154, 161f
Isolated carpal bones
complications, 21
dorsal fracture-dislocations, 21, 22f
lunate fractures, 21
pisiform fractures, 21
Signet ring sign, 21
triquetral fractures, 21, 21f
vertical/transverse fractures, 21
J
Joint aspiration
Gram stain, 485
hip arthroplasty aspiration, 485–486, 489
intra-articular position, 484
iodinated contrast medium, 485
septic arthritis, 484
sterile synovial fluid, 485
Joint infections, 431–433, 434f–435f
with hallux rigidus, elderly, 479, 480f
single-plane fluoroscopic equipment, 479
treatment, 481
ultrasonography, 479
Joint injections
with hallux rigidus, elderly, 479, 480f
single-plane fluoroscopic equipment, 479
treatment, 481
ultrasonography, 479
Joint replacement arthroplasty, 515f
Jumper’s knee, 99, 100f
Juvenile chronic arthritis, 277, 280f
Juvenile idiopathic arthritis, 311, 312f–313f
Juxta-articular osteoporosis, 297, 299f, 301
K
Kienbock disease, 447–448, 450f
Knee
antibiotic-loaded cement spacer, 514f
arcuate fracture, 45
Baker cyst, loose bodies, 508f
bone marrow conditions at, 444, 445f
chondrocalcinosis, 277, 279f
chronic pain, 518f
effusion, 47, 472, 473f
floating knee, 47
injuries
anterior and posterior central root ligaments, 83
anterior cruciate ligament (ACL) injury, 94, 94f–96f
articular cartilage injury, 102, 102f–103f
axial T2 FS MRI, 81, 84f
bone bruise patterns, 101–102
capsular structures, 84
circumferential bundles, 83
collagen bundles, 83
coronal T1 MRI anatomy, 81, 82f
cruciate ligaments, 81–82, 82f
dynamic stabilizers, 81
extensor mechanism injury, 83. See also Extensor mechanism injury
fat pad edema, 104, 105f
Hoffa fat pad, 85
Humphrey ligament, 83
hyaline articular cartilage, 87
iliotibial (IT) band syndrome, 104, 104f
intermeniscal ligaments, 83, 86f
lateral femoral condyle, 81
lateral patellar dislocation, 101, 101f
ligament injury biomechanics, 92–94, 94f
medial collateral ligament (MCL) injury, 96, 97f
medial femoral condyle, 81
medial meniscus (MM), 83
medial patellar facet, 87
meniscal roots, 81, 83, 85f
meniscal tears. See Meniscal tears
meniscomeniscal ligaments, 83
MRI protocol, 81
multiligament injury, 99, 99f–100f
myotendinous injury, 102–104, 103f
patellofemoral ligaments, 83
pes anserinus bursitis, 104, 105f
plica syndrome, 104, 104f
popliteus muscle, 84
posterior cruciate ligament (PCL) injury, 95, 96f–97f
posterolateral corner injury, 97, 98f
posteromedial corner injury, 97, 98f
prefemoral fat pad, 85
sagittal PD FS MRI, 81, 83f
soft-tissue structures, 81
static stabilizers, 81
subchondral bone, 87
synovial cavity, 84–85
tibial plateaus, 82
transverse intermeniscal ligament, 83, 86f
Wrisberg ligament, 83
intercondylar fracture, 45
lateral meniscus, radial tear, 498f
osteoarthritis, 285, 285f–288f
Paget disease (osteitis deformans), 418, 418f, 518f
parosteal osteosarcoma, 525f
patella alta, 47
patella baja, 47
patellar dislocations, 46
pyrophosphate arthropathy of, 316, 318f
rheumatoid arthritis (RA), 299, 302f, 511f
Segond fracture, 45
Stellate fractures, 47
Stieda fracture, 45
stress fracture, 525f
subchondral insufficiency fracture, 446–447, 449f
bicondylar total knee replacement (TKR), 358–359, 360f
extensor realignment, 358, 358f–359f
femur fracture, 359, 363f
intercondylar-stabilized total knee replacement, 359, 361f
metal synovitis, 360, 363f
osteolysis, 360, 364f
osteotomy, 358, 359f
patellar component, 359, 362f
polyethylene loss, 360
polyethylene thinning, 359, 363f
rotating hinge total knee replacement, 359, 361f
synovial discoloration, 360
unicompartmental total knee replacement, 359, 362f
transient lateral patellar dislocation, 498f
ultrasound, 469, 472, 473f
vascular and nerve injuries, 45
L
Labral tears, 118, 121, 121f
Lacertus fibrosus, 142
Lamellar bone, 2
Langerhans cell histiocytosis (LCH), 220–221, 220f
Latent lesions, 198
Lateral epicondylitis (tennis elbow), 140, 142f
Lateral femoral condyle, 81
Lateral foot alignment, 331, 333f
Lateral meniscus tear, with meniscal cyst, 322, 324f
Lateral patellar dislocation, 101, 101f
Lateral ulnar collateral ligament (LUCL), 135, 136f, 140, 141f
Leaguer’s elbow, 138, 140f
Legg-Calvé-Perthes disease, 286, 291f
Legg-Perthes disease, 350, 352f
Leprosy, 441, 442f
Lesser toe deformities, 345, 347f
Lidocaine, 479
Ligament injury biomechanics, 92–94, 94f
Limb girdle muscular dystrophy, 263, 273f
Lipoma arborescens, 327, 329f
Lipomas, 257–258, 261f–263f, 508f
flexor arm, 257–258, 261f
in posterior thigh compartment, 257–258, 262f
spindle-cell lipoma, 257–258, 263f
Liposarcoma, 256, 259f
Lisfranc injury, 525f
joint sprain, 185, 188f
ligament anatomy, 184, 188f
stages of, 185
Lisfranc joint, 331
Loading, 1, 2f, 494f
direct loading, 2
fractures, 2–4
indirect loading, 2–3
longitudinal compressive loading, 3
rotational loading, 3
types, 2–3, 3f
Local anesthetics
bupivacaine, 481
lidocaine, 479, 481
Lower extremity fractures
acetabular fractures, 39–41, 42f–43f
ankle mortise, 48–52, 51f–54f
calcaneus, 53–54, 57f–58f
forefoot, 54–56, 58f–61f
hip dislocations, 41–42, 44f, 45f
intertrochanteric fractures, 43, 46f
intracapsular fractures, 42–43, 45f, 46f
knee, 45–47, 47f–49f
midfoot, 54, 58f
pelvic ring, 38
anatomy, 38
stable fractures, 38, 39f
unstable injuries, 38–39, 40f–42f
proximal femur, 42
shaft and distal femur fractures, 44–45, 47f
subtrochanteric fractures, 43–44, 46f–47f
talus, 52, 55f–56f
tibial plateau, 47, 49f–50f
tibial shaft, 47, 51f
LUCL (lateral ulnar collateral ligament), 135, 136f, 140, 141f
Lumbar spine, 245, 246f, 405–406, 406f
Lung carcinoma, 245, 246f, 250, 251f
Lunotriquetral ligaments, 164, 165f, 170
Luteus maximus, 146
Lyme disease, 440–441
Lymphoma, intramuscular, 257, 261f
Lysosomal storage disorders, 456, 457f–458f
Lytic lesions, 243
Lytic metastases, 243, 244f
M
Macrodystrophia lipomatosa, 392, 393f
Madelung deformity, 401–402, 402f
Maffucci syndrome, 210, 393, 395f
Malignant bone tumors
adamantinoma, tibia, 234, 240f, 507f
anaplastic sarcoma, 227
central chondrosarcoma, 225, 231f
chordoma, 233–234, 239f
diffuse large B-cell lymphoma, 228, 235f
Ewing sarcoma
of distal humerus, 230, 237f
femoral shaft, 230, 238f
of lower extremities, 229
of rib, 230, 238f
exostotic (peripheral) chondrosarcomas, 226, 233f
Hodgkin lymphoma, 228–229, 236f
low-grade chondrosarcoma, 225, 232f
multiple myeloma, 227–228, 234f
features, 228, 234t
osteosarcoma
clinical features, 225
conventional (intramedullary) osteosarcoma, 224, 226f
fracture callus, 224
high-grade surface osteosarcoma, 225, 231f
mineralized osseous matrix, 224
neoadjuvant chemotherapy, 225
parosteal osteosarcoma, 225, 230f
proximal tibia, 224, 227f
radiation-induced osteosarcoma, 225, 228f
with skip metastasis, 224, 227f
telangiectatic osteosarcoma, 225, 229f
types, 224, 225t
soft-tissue density, 226
solitary myeloma (plasmacytoma), 228, 235f
undifferentiated high-grade pleomorphic sarcoma, 232–233, 239f
Malignant fibrous histiocytoma (MFH), 232
Malignant lesions, 198–199
Malignant radiation-induced tumors, 252
Malunion, 74
Marfan Syndrome, 393, 395, 395f
Marginal osteophyte, 277, 278f
Marrow space metastasis, 245, 246f
Massive allograft bone, 372
Matrix calcification, 210–211
Matrix mineralization, 195, 197, 197t
MCL (medial collateral ligament) injury, 96, 97f
MCP (metacarpophalangeal) joint, 164, 296–297, 298f
Medial apophysitis, 138, 140f
Medial collateral ligament (MCL) injury, 96, 97f, 500f
Medial epicondyle apophysitis, 138, 140f
Medial epicondylitis (Golfer’s elbow), 140–141, 142f, 465, 466f
Medial femoral condyle, 81
Medial impingement syndromes, 180
Medial meniscus (MM), 83
Medial patellar facet, 87
Median neuropathy, 174, 174f
Medullary bone infarcts, 448, 452f
Melorheostosis, 401, 401f
Meniscal cysts, 87
lateral meniscus tear with, 322, 324f
Meniscal roots
axial MRI, 81, 85f
coronal PD FS MRI, 83, 85f
Meniscal tears
acute knee injury, 88, 90f
arthroscopic meniscal surgery, 92
bucket handle meniscal tear, 88, 89f
classification, 87
direct posterior root avulsions, 91
discoid lateral meniscus, 92, 93f
discoid lateral meniscus with tear, 92, 93f
floating medial meniscus (MM), 92, 92f
horizontal lateral meniscal tear, 87, 87f
horizontal tears, 87, 87f
lateral meniscal bucket handle tears, 88, 90f
lateral meniscal flap tear, 88, 88f
lateral meniscus radial tear, 88–89, 91f
longitudinal tears, 88, 88f
medial meniscal root, 91, 92f
meniscal hoop strength, 89
meniscocapsular separation, 91–92, 92f
meniscotibial (coronary) ligament, 92
MRI findings of, 87
partial meniscectomy/meniscal repair, 91
peripheral vertical medial meniscal tear, 88, 89f
Wrisberg rip, 88, 90f
Merkel cell carcinoma, 250, 251f
Metabolic deposition diseases
amyloid arthropathy, 321, 321f
multicentric reticulohistiocytosis, 321, 321f
tophaceous gout
in carpus, 319, 320f
dual-energy CT (DECT), 319, 320f
in hand, 319, 320f
hyperuricemia, 319
in midfoot, 319, 320f
monosodium urate crystals, 319
overhanging edges and chronic erosions, 319, 320f
patient management, 321
Metacarpophalangeal (MCP) joint, 164, 296–297, 298f, 515f
Metal artifact reduction algorithm, 199
Metal prostheses, 354
Metal synovitis, 360, 363f
Metastatic bone tumors, 242
Metastatic osteosarcoma, 199, 201f–202f
Metatarsophalangeal (MTP) joint, 176, 314
hypertrophic osteoarthritis, 479, 480f
Methotrexate, 419
MFH (malignant fibrous histiocytoma), 232
Midcarpal joint, 163
Midfoot, 331
Midsubstance/intrasubstance tear, 121
Mineral disorder, 262, 271f–272f
Mineral metabolism, abnormal
acute osteoporosis, 407–408, 408f
bone mineral densitometry, 405–407, 406f–407f, 406t, 408t
complex regional pain syndrome, 408
hydroxyapatite crystals, 409
hyperparathyroidism. See Hyperparathyroidism
osteomalacia. See Osteomalacia
parathyroid hormone, 409
primary osteoporosis (involutional osteoporosis), 404–405, 405f
regional migratory osteoporosis, 408–409
renal glomerular filtration rate, 409
secondary osteoporosis, 407, 408t
trabecular structure, 404
transient regional osteoporosis, 408, 408f
MM (medial meniscus), 83
Monostotic fibrous dysplasia, 213, 215f
Monteggia fracture, 25, 27, 28f, 496f
Morel-Lavallée lesion, 261–262, 269f
Morton neuroma, 345, 346f
Moth-eaten bone destruction, 192, 194f
Mottled sclerosis, 193
MTP (metatarsophalangeal) joint, 176, 314
Multiligament injury, 99, 99f–100f
Multiligament knee injuries, 95
Multiple blastic metastases, 244, 246f
Multiple enchondromas, 210, 393, 394f–395f
Multiple enchondromatosis (Ollier disease), 210, 211f
Multiple hereditary exostoses, 395–396, 396f–397f
Multiple marrow infarcts, 448, 451f, 520f
Multiple myeloma, 192, 227–228, 234f
features, 228, 234t
Multiple osteochondromas, 208
Multisystem fibrosing autoimmune connective tissue disease, 302
Muscle fascicles, 461
Muscular dystrophy, 263, 273f
Musculoskeletal Tumor Society, 198–199, 257
Myelofibrosis, 454–456, 456f–457f
Myeloma, 202, 202f
Myositis, 301
Myositis ossificans, 262, 270f
Myotendinous injury, 102–104, 103f, 523f
Myotendinous junction, 121–122
Myxoid liposarcoma, 255, 257f
Myxoid matrix, 197
Myxomas, 261
N
National Organization for Rare Diseases, 390
Necrotic bone fragments, 74
Necrotizing soft-tissue infection (NSTI), 438–439, 440f–441f
Nephrogenic fibrosing dermopathy, 421–422, 424f
Nephrogenic systemic fibrosis (NSF), 421–422, 424f, 481
Neurofibroma, 258–259, 266f
Neurofibromatosis, 397, 397f–398f
in adult, 258–259, 267f
Neuropathic osteoarthropathy, 314, 315f, 332–333, 336f–337f
NIH Office of Rare Disease Research, 390
Nonendocrine adrenocorticotropic hormone–producing tumors, 415
Nonerosive symmetric polyarthritis, 301
Non–fat-suppressed pulse sequences, 81
Noninflammatory joint disease
crystal-associated diseases. See Crystal-associated diseases
cuff tear arthropathy, 326–327, 327f–328f
femoroacetabular impingement (FAI)
acetabular labral pathology, 323
cam- and pincer-type FAI, 323, 326f
crossover sign, 323, 325f
femoral head-neck junction, 323, 325f
os acetabula, 323, 325f
synovial herniation pit, 323, 325f
lipoma arborescens, 327, 329f
metabolic deposition diseases. See Metabolic deposition diseases
neuropathic osteoarthropathy, 314, 315f
osteolysis, distal clavicle, 322, 324f
pigmented villonodular synovitis (PVNS), 321–322, 322f–323f
shoulder impingement
posterosuperior impingement, 326, 327f
subacromial impingement, 326, 326f
synovial cysts, 322, 324f
Nonossifying fibroma, 212–213, 214f
Nonsteroidal anti-inflammatory drugs (NSAIDs), 206, 207f
Nora lesion, 209
NSF (nephrogenic systemic fibrosis), 421–422, 424f, 481
NSTI (necrotizing soft-tissue infection), 438–439, 440f–441f
O
Occam’s Razor vs. Hickam’s Dictum, 281–282
Occult hip fractures, 147
Occult primary tumors, 242
OCD (osteochondral disease), 139, 140f
Odontoid process, 300–301, 304f
Olecranon bursae, 136–137, 137f
Olecranon recess, 134
Olecranon stress
fracture, 137
injuries, 139, 141f
Oligoarthritis, symmetric, 309
Ollier disease (multiple enchondromatosis), 210, 211f, 393, 394f
Online Mendelian Inheritance in Man (OMIM) site, 389
Open fractures, 495f
closed fractures, 8
type I, 8, 9f
type II, 8, 9f
type III, 8, 9f
Osseous metastases, 250
Osseous structures, 164
Ossicles/sesamoids injuries, 182
Os styloideum, 168, 168f
Osteoarthritis, 322
articular cartilage, 283, 284f
carpometacarpal joint, 510f
degenerative spine conditions
ankylosing spondylitis, 290, 293f
annulus fibrosus, 288
degenerative disk disease, 289
degenerative lumbar disk herniation, 289, 292f
diffuse idiopathic skeletal hyperostosis (DISH), 290, 293f–294f
intervertebral disk joints, 287–288, 291f
lumbar degenerative disk disease, 289, 292f
spondyloarthropathies, 290
spondylosis deformans, 289, 292f
hand, inflammatory (erosive), 287, 291f, 510f
hip, 285, 288f, 510f
horizontal tear, 87
knee, 285, 285f–288f
prevalence, 283
primary osteoarthritis
bone abnormalities, 284–285, 284f–285f
cartilage abnormalities, 284
synovial joints, 283
radiology of, 276
rheumatoid arthritis (RA), 296
secondary osteoarthritis, 283
developmental dysplasia, 286, 291f
factors, 286
fibrocartilage scar, 286
inflammatory arthritis, 286
Legg-Calvé-Perthes disease, 286, 291f
posttraumatic ankle osteoarthritis, 286, 290f
shoulder, 285, 288f–289f
spine, 286, 290f
subchondral sclerosis, 523f
Osteoblastic metastases, 205, 249
Osteoblastoma
aneurysmal bone cyst (ABC) formation, 208
cortical expansion and destruction, 208
diaphysis/metaphysis, 208
osteoid-forming neoplasms, 207
osteoid matrix mineralization, 208
recurrence rate, 208
sclerotic border, 208, 208f
superficial lesions, 207
Osteochondral disease (OCD), 139, 140f
Osteochondroma (exostosis), 504f
bizarre parosteal osteochondromatous proliferation (BPOP), 209–210, 211f
with cartilage cap, 208, 210f
chondrocytes, 208
complications of, 208
digital extensor mechanism, 210
dysplasia epiphysealis hemimelica, 208
endochondral ossification, 208
hereditary multiple exostoses, 208, 208f
nonmineralized cartilage, 209
pedunculated osteochondroma, 208, 209f
peripheral and septal enhancement, 209
sessile osteochondroma, 208, 209f
solitary/multiple, 208
subungual exostosis, 209–210
turret exostosis, 209
Osteoclastic bone resorption, 409
Osteoclast-stimulating factors, 243
Osteogenesis imperfecta, 397–398, 398f–399f, 516f
Osteoid matrix, 197, 197f, 208
Osteoid osteoma
bone density, 206
double-density sign, 206
18F-FDG PET, 206
fusiform cortical thickening, 206
intra-articular osteoid osteomas, 206
intracortical osteoid osteomas, 206
nidus, 206
nonsteroidal anti-inflammatory drugs (NSAIDs), 206, 207f
periarticular osteopenia, 206
periosteal reaction, 206
radiofrequency (RF) ablation, 207
reactive sclerosis, 206
residual/recurrent tumor, 207
scoliosis, 206
T1 signal and variable T2 signal, 206, 207f
Osteoinductive humoral factors, 243
Osteolysis, 354–355, 357f, 360, 364f
distal clavicle, 322, 324f
total hip replacement, 514f
Osteomalacia
renal osteodystrophy, 413, 413f
vitamin D deficiency, 411–412, 412f
vitamin D physiology and function, 410–411, 412f
Osteomyelitis, 333
acute
in diabetic, 428, 430f
in distal fibula, 428, 430f
in distal phalanx and distal interphalangeal joint, 428, 431f
distal tibia, 429, 432f
in femur, 428, 429f
infection resolution, 429, 432f
in proximal humerus, 428, 429f
right ischial tuberosity, 429, 431f
soft-tissue swelling, 428
treatment, 429
bone marrow signal abnormality, 520f
chronic, 429–431, 432f–433f
forearm, 519f
Osteonecrosis, 20, 148, 151f, 252, 301, 520f
anteroposterior radiograph, 448, 451f
calcified marrow infarcts, 449, 452f
femoral head
alcoholism and systemic corticosteroids, 444
avascular necrosis, 446, 448f
clinical conditions, 444, 446t
with crescent sign, 445, 447f
with marrow edema, 445, 448f
predominant blood supply, 444
sclerosis, 445, 446f
with subchondral collapse, 445, 447f
with subchondral fracture, 446, 449f
weight-bearing surface, 445
hypercortisolism, 415–416
Kienbock disease, 447–448, 450f
medullary bone infarcts, 448, 452f
multiple marrow infarcts, 448, 451f
pathophysiology, 448
periosteal portion, 444
subchondral insufficiency fracture, knee, 446–447, 449f
Osteopathia striata, 400–401, 401f
Osteopetrosis, 398–400, 399f–400f, 516f
Osteopoikilosis, 400, 400f
Osteoporosis, 517f
abnormal mineral metabolism
acute osteoporosis, 407–408, 408f
bone mineral densitometry, 405–407, 406f–407f, 406t, 408t
complex regional pain syndrome, 408
hydroxyapatite crystals, 409
hyperparathyroidism. See Hyperparathyroidism
osteomalacia. See Osteomalacia
parathyroid hormone, 409
primary osteoporosis (involutional osteoporosis), 404–405, 405f
regional migratory osteoporosis, 408–409
renal glomerular filtration rate, 409
secondary osteoporosis, 407, 408t
trabecular structure, 404
transient regional osteoporosis, 408, 408f
bisphosphonate insufficiency fracture, 518f
hypercortisolism, 415, 416f
Osteosarcoma, 245, 248f, 506f, 524f
Codman triangle, 523f
malignant bone tumors
clinical features, 225
conventional (intramedullary) osteosarcoma, 224, 226f
fracture callus, 224
high-grade surface osteosarcoma, 225, 231f
mineralized osseous matrix, 224
neoadjuvant chemotherapy, 225
parosteal osteosarcoma, 225, 230f
proximal tibia, 224, 227f
radiation-induced osteosarcoma, 225, 228f
with skip metastasis, 224, 227f
telangiectatic osteosarcoma, 225, 229f
types, 224, 225t
metastases, 249
Osteotomy, hip surgery
fracture malunion, 350
innominate osteotomy, 350, 352f
lateral displacement osteotomy repositions, 350
limb rotation evaluation, 350, 351f
rotational osteotomy, 350, 352f
valgus osteotomy, 350, 351f
P
Paget disease (osteitis deformans), 518f
in femur, 418, 419f
insufficiency fractures, 418, 419f
ivory vertebra, 418, 419f
at knee, 418, 418f
paramyxoviral infection, 417
in pelvis, 418, 420f
picture-frame vertebra appearance, 418, 418f
progression of, 417, 418f
trabecular appearance, 417
Pain, 479
Panner disease, 139
Pannus, 277
rheumatoid arthritis (RA), 296, 298
Paraplegia, 388
Parasitic infestation, 440, 441f
Parosteal osteosarcoma, 225, 230f, 525f
Patellar tendon tear, 101, 101f
Patellofemoral ligaments, 83
PCL (posterior cruciate ligament) injury
dashboard injury, 95, 96f
injury, 95, 96f
midsubstance tears, 95
mucoid degeneration, 95, 97f
Pedunculated osteochondroma, 208, 209f
Pelvic ring
anteroposterior (AP) radiograph, 38
central hip dislocation, 39
isolated fractures, 38
sacroiliac (SI) joints, 38
sacrospinous ligaments, 39
sacrotuberous ligaments, 39
stable fractures, 38
stress fractures, 38
strong interosseous ligament, 38
urologic injuries, 39
vertical shear forces, 39
Pencil-in-cup erosions, 309, 309f
Percutaneous CT-guided biopsy
bone lesions, 486, 488, 490, 490f–491f
complications, 486, 490t
metastatic lesions, 486
soft-tissue lesions, 486, 490f
Periarticular calcinosis, 420
hemodialysis, 262, 272f
Periarticular osteopenia, 206
Periarticular osteoporosis, 299
Perilunate injuries, 22t
dislocation, 21–22, 24f–25f
hyperextension, 21
intercarpal supination, 21
midcarpal dissociation, 22, 24f
radiographic signs, 22
rotary subluxation, 21, 23f
scapholunate dissociation, 21
space of Poirier, 21–22
triquetral dislocation, 22
ulnar deviation, 21
Periosteal chondroma, 210, 212f
Periosteal reaction layers, 193, 195f
Peripheral longitudinal tears, 88
Peripheral nerve sheath tumors
neurofibroma, 258–259, 266f
neurofibromatosis, in adult, 258–259, 267f
schwannoma, 258–259, 266f
Periprosthetic soft-tissue lesions, 356
Peritendinitis, 173
Permeated bone destruction, 192, 194f
Pes anserinus bursitis, 104, 105f
Pigmented villonodular synovitis (PVNS), 321–322, 322f–323f
Pin infections, 76
Piriformis syndrome, 155, 502f
Plantar aponeurosis, 339
Plantar fasciitis, 339, 339f
Plates
blade plate, 71, 71f
buttress plates, 69, 70f
compression, 69
cortical plates, 69, 70–71, 71f
distal radius fixation, 70, 71f
dynamic compression, 69, 70f
interfragmentary screws, 70
locking plates, 69, 70f
neutralization plates, 70
small plates, 69
static compression, 69
Pleomorphic sarcoma, 255, 256f
Plica syndrome, 104, 104f, 138
Polyarthritis, 309
Polyarticular arthropathy, 510f
Polydactyly, 391, 392f
Polyethylene acetabular liner, 356
Polyethylene osteolysis, 515f
Polymyositis, 302–303, 306f
Polyostotic fibrous dysplasia, 214, 215f
Popliteal artery entrapment syndrome, 274f
Popliteus muscle, 84
Postarthroplasty hip, 153–154, 161f
Posterior cruciate ligament (PCL) injury
dashboard injury, 95, 96f
injury, 95, 96f
midsubstance tears, 95
mucoid degeneration, 95, 97f
Posterior interosseous nerve syndrome, 144, 144f
Posterior talofibular ligaments (PTFL), 176, 178f
Posterolateral corner injury, 97, 98f
Posteromedial corner injury, 97, 98f
Postmenopausal osteoporosis, 404
Postsurgical lower extremity
ankle surgery. See Ankle, surgery and replacement
hip surgery. See Hip, surgery and replacement
knee surgery. See Knee, surgery and replacement
tumor reconstruction. See Tumor reconstruction
Postsurgical upper extremity. See Arthroplasty
Posttraumatic subcutaneous hematoma, 261–262, 269f
Prefemoral fat pad, 85
Primary malignant bone tumors, types, 192, 193t
Primary sarcoma, 192
Primitive neural ectodermal tumor, 255, 257f
Progressive osteoarthritis, 169–170
Prostate carcinoma
diffuse blastic metastases, 243, 245f
pathologic avulsion fracture, 249, 250f
Proximal femur
elderly patients, 42
femoral fractures, 42
intertrochanteric fractures, 42
osteoporotic femurs, 42
preexisting insufficiency, 42
Proximal femur fractures, 146
Proximal interphalangeal (PIP) joint, 164, 296
Proximal tibial metaphysis, 522f
Pseudoachondroplasia, 391, 391f
Psoriatic arthritis
feet, 309, 310f
HLA-B27, 309
inflammatory periostitis, 309, 310f
interdigitating erosions, 309, 309f
polyarthritis, 309
sacroiliitis and spondylitis, 309
“sausage digit” swelling, 309, 309f
spine and sacroiliac joints, 310, 310f
symmetric oligoarthritis, 309
symmetric seronegative polyarthritis, 309
PTFL (posterior talofibular ligaments), 176, 178f
PubMed search, 389
Pulley lesions, 114, 115f
Punctate cartilage matrix mineralization, 197, 198f
PVNS (pigmented villonodular synovitis), 321–322, 322f–323f
Pyomyositis, 438, 439f–440f, 519f
Pyrophosphate arthropathy
calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, 316,
316f, 318f
of knee, 316, 318f
with scapholunate advanced collapse wrist, 316, 316f
Q
Quadratus femoris muscle, 154–155
Quadriceps mechanism, 92, 104
Quadriceps tendon tears, 101, 101f
Quadriplegia, 388
R
RA. See Rheumatoid arthritis (RA)
Radial collateral ligament (RCL) recess, 134
Radiation-induced osteosarcoma, 225, 228f
Radiocarpal joint, 163
Radiocarpal ligaments, 164
Radionuclide bone, 153, 507f
Radioscaphocapitate, 164
Radioulnar ligaments, 164, 165f
Recombinant DNA technology, 297
Rectus femoris muscle, 152, 155f
Recurrent parosteal osteosarcoma, 199, 201f
Recurrent soft-tissue sarcoma, 199, 201f
Regional acceleratory phenomenon, 449
Renal glomerular filtration rate, 409
Renal osteodystrophy, 413, 413f
Retrocalcaneal bursa, 299, 303f
Reverse Colles fracture, 22
Reverse total shoulder replacement, 372, 374f
with scapular notch, 372, 374f
Rhabdomyolysis, 264, 274f
Rheumatism, 276
Rheumatoid arthritis (RA), 277
acromioclavicular joint, 299
of carpal bones, 298, 300f
clinical course, 296
clinical diagnosis, 296
clinical outcomes, 297
compressive erosions and remodeling, 297
disease-modifying antirheumatic drugs (DMARDs), 297
distal interphalangeal, 512f
extra-articular manifestations, 300, 304f
foot, 299, 303f
fusiform soft-tissue swelling, 297
gadolinium, 297
genetic factors, 296
glenohumeral joint, 299
hand deformities, 297, 299f
hip, 299, 303f
juxta-articular osteoporosis, 297, 299f
knees, 299, 302f, 511f
metacarpophalangeal (MCP) erosions, 297, 298f
metacarpophalangeal (MCP) joint, 296
metatarsophalangeal and toe joints, 277, 279f
osteoarthritis, 296
pannus, 296, 298
pathologic change in, 296
periarticular osteoporosis, 299
proximal interphalangeal (PIP) joint, 296
recombinant DNA technology, 297
retrocalcaneal bursa, 299, 303f
rheumatoid factor (RF), 296
rheumatoid hand, 297, 297f
of ring finger, 297, 298f
secondary degenerative changes, 297
with osteoporotic bones, 299, 301f
silicone material, joint replacement arthroplasty, 515f
spine
atlantoaxial subluxation, 300–301, 303f
odontoid process, 300–301, 304f
thoracic and lumbar spine, 300
spontaneous Achilles tendon rupture, 299
subchondral bone marrow edema, 297
synovial hyperemia, 296
synovial hypertrophy and effusion, 299
synovial joints, 296
treatment of, 297
wrist, 296, 298, 300f
with tenosynovitis, 298, 301f
Rheumatoid factor (RF), 296
Rings-and-arcs cartilage matrix mineralization, 197, 198f
Rockwood type I, 125, 129f
Rockwood type II, 125, 130f
Rockwood type III, 125, 130f
Rockwood type IV, 129, 131f
Rockwood type V, 129
Rockwood type VI, 129
Rotator cuff
abduction, 111
angle artifact, 112, 114
coronal and transverse planes, 111
infraspinatus muscle, 109
MR pulse sequences, 112
pathology, 121–122, 122f–124f
calcific tendinosis, 122, 124f
coracoacromial arch, 121
dynamic stabilization, 121
full-thickness rotator cuff tear, 121, 123f
hydroxyapatite crystal deposition disease, 122
infraspinatus tendon, 121
partial-thickness rotator cuff tears, 121, 123f
soft-tissue calcific deposits, 122
spectrum of, 121, 122f
subacromial-subdeltoid (SA-SD) bursitis, 122, 124f
teardrop-shaped/nodular lesions, 122
tendinopathy, 121, 123f
tendon articular/bursal surface fibers, 121
subscapularis, 499f
superior humeral head displacement, 111
suprapinatus muscle, 109
teres minor muscle, 109
time to echo (TE), 112
Rotator interval capsule, 114
S
Sacroiliitis, 307, 308–309, 308f, 309, 309f, 310
Sagittal band rupture, 172, 172f
Salto-Talaris prosthesis, 362, 365f
Sarcoidosis, 423–424, 425f–426f
“Sausage digit” swelling, 309, 309f
Scaphoid, 20, 20f, 169, 169f
Scapholunate advanced collapse wrist, 170, 171f
pyrophosphate arthropathy with, 316, 316f
Scapholunate ligaments, 164, 165f, 169
Scars, 76
Schatzker classification, 47
Scheker prosthesis, 378
Schwannoma, 258–259, 266f
Scleroderma, 302, 305f
Sclerosis, 278, 445, 446f
Sclerotic bone lesions, 205, 249
Scoliosis, 206
Screws, 497f
Acutrak screw, 65, 67f
ankle fracture with internal fixation, 65, 67f
bioabsorbable screw, 65, 67f
cancellous bone, 64
cannulated screws, 65, 67f
dynamic compression, 63
dynamic hip screws, 67, 68f
hexagonal shaft driver, 64
orthopedic screws, 64, 66f
Septic arthritis, 431–433, 434f–435f
Septic bursitis infection, 123
Seronegative polyarthritis, symmetric, 309
Seronegative spondyloarthropathy, 304
Sesamoiditis, 342, 343f, 523f
Sesamoids, 185, 189
Sessile osteochondroma, 208, 209f
Severe pes planovalgus, 332, 334f
SGHL (superior glenohumeral ligament), 108, 110f
Shaft and distal femur fractures, 44–45, 47f
intercondylar fractures, 45
osteoporosis, 45
young adults, 44
Short tau inversion recovery (STIR), 107
Shoulder
arthroplasty
anatomic shoulder hemiarthroplasty, 371, 373f
anatomic total shoulder replacement, 371, 373f
Grashey view, 371
multidirectional glenohumeral subluxation, 372
oncologic (modular) proximal humerus replacement, 372, 375f
partial shoulder resurfacing hemiarthroplasty, 371, 372f
primary indication, 371
resurfacing hemiarthroplasty, 371, 372f
reverse total shoulder replacement, 372, 374f
rotator cuff function, 371
calcium pyrophosphate dihydrate deposition disease, 509f
injection, 481–482, 482f–483f
injuries
acromioclavicular joint (ACJ), 114, 116f. See also Acromioclavicular joint
(ACJ)
biceps brachii muscles and tendons, 114, 114f, 124–125, 126f–127f
biceps reflection pulley, 114, 115f
Buford complex, 109, 112f
glenohumeral instability. See Glenohumeral instability
glenohumeral joint anatomy, 107–108, 108f
glenohumeral ligaments, 108, 110f
glenoid fossa, 108
glenoid hyaline cartilage articular surface, 108
glenoid labrum, 108, 109f
intermediate-weighted PD sequences, 108
labral tears, 118, 121, 121f
MRI shoulder protocol, 107
rotator cuff, 113f. See also Rotator cuff
subacromial-subdeltoid (SA-SD) bursa, 114, 116, 118f, 123
sublabral foramen/hole, 109, 112f
sublabral recess/sulcus, 109, 111f
superior labrum anteroposterior (SLAP) lesion, 109
supraglenoid tubercle, 109
3Tesla (3T) MRI study, 108
neuropathic joint, 314, 315f
osteoarthritis, 285, 288f–289f
pathologic fracture, 526f
posterior shoulder dislocation, 495f
posterosuperior impingement, 326, 327f
pyrophosphate arthropathy of, 316, 318f
reverse shoulder prosthesis, anterior dislocation, 515f
rheumatoid arthritis (RA) of, 299, 301f
with osteoporotic bones, 299, 301f
subacromial impingement, 326, 326f
superior glenohumeral ligament, 522f
ultrasound
acromioclavicular joint, 462, 462f
biceps dislocation, 461, 462f
biceps tendon, 461, 461f
complete rotator cuff tear of, 462, 464f
infraspinatus tendon, 462, 464f
partial rotator cuff tear, 462, 463f
posterior glenohumeral joint, 462, 465f
spinoglenoid notch paralabral cyst, 463, 465f
subdeltoid-subacromial bursitis, 462–463, 465f
supraspinatus tendinosis, 462, 464f
supraspinatus tendon partial tear, 462, 464f
teres minor tendon, 462, 465f
Sickle cell disease, 452, 454f, 520f
Sinus tarsi ligaments, 176, 181
Sinus tarsi syndrome, 340–341, 340f
Skeletal developmental disorder, nonhereditary, 208
Skeletal fluorosis, 421, 421f
Skeletal metastases, 242, 243t
Skin, lidocaine solution, 479
Skin ulcer, 518f
SLAP (superior labrum anteroposterior) labral tear, 109, 118, 121, 121f
SLE (systemic lupus erythematosus), 301–302, 305f
Smith fracture, 22
Soft-tissue atrophy, 76, 302
Soft-tissue biomechanics
creep, 5
direct trauma, 6
fibrocartilage articular, 7
hematomas, 6–7
hemorrhage and acute inflammation, 6
sprains, 5, 7t
sterile collections, 6–7
strains, 5, 7t
stress relaxation, 5
subcutaneous avulsion, 6
superficial abrasions, 6
tears, 5
viscous effects, 5
Soft-tissue calcification
chronic kidney disease
periarticular calcinosis, hemodialysis, 262, 272f
in skin and subcutaneous tissues, 262, 271f
primary tumoral calcinosis, 262–263, 272f
Soft-tissue healing
direct repair, 73
proliferating granulation, 73
repair, 73
soft-tissue anchors, 73, 74f
tendon and ligament healing, 73
Soft-tissue hemangiomas, 210
Soft-tissue injuries
abnormal intrasubstance signal/swelling, 7
achilles tear, 8, 8f
edema, 7
fluoroscopy, 7, 7f
hemorrhage, 7
kinematic observation, 7
ligaments tears, 7
muscle tears, 7
sonography, 7
tendon tears, 7, 8
Soft-tissue metastases
factors, 250
from lung cancer, 250, 251f
from Merkel cell carcinoma, 250, 251f
to muscle, 250, 251f
Soft-tissue sarcomas, 199, 200f
AJCC prognostic stage groups, 256, 260t
Baker cyst, 260, 267f
benign lesions
aggressive fibromatosis, 259–260, 267f
elastofibroma, 258, 264f
giant cell tumor, tendon sheath, 258, 265f
hemangioma, 258, 264f
lipomas, 257–258, 261f–263f
peripheral nerve sheath tumors, 258–259, 266f–267f
biological grade of, 255
bursitis, 260–261, 268f
extremities and limb girdles, 255, 256t
ganglion cyst, 260, 267f
incidence of, 255
intramuscular lymphoma, 257, 261f
lesion’s size and location, 256
liposarcoma, 256, 259f
Musculoskeletal Tumor Society surgical staging system, 257
myxoid liposarcoma, 255, 257f
myxomas, 261
pleomorphic sarcoma, 255, 256f
posttraumatic masses
calcific myonecrosis, 262, 271f
hematomas, 261–262, 269f
Morel-Lavallée lesion, 261–262, 269f
myositis ossificans, 262, 270f
preoperative staging, 256, 260f
primary, 509f
primitive neural ectodermal tumor, 255, 257f
subcutaneous/intermuscular fat, 256
synovial cysts, 260
synovial sarcoma, 256, 258f
World Health Organization classification, 255
Soft-tissue swelling, 20, 277–278, 280f–281f
hypertrophic osteoarthritis, 479, 480f
psoriatic arthritis, 509f
Solitary bone lesion, 202, 202f–203f
back pain, 202, 203f
humeral head pseudolesion, 202, 202f–203f
longitudinal locations, 192, 193t
myeloma, 202, 202f
nonaggressive, 504f
transverse locations, 192, 193t
Solitary enchondroma, 210
Solitary myeloma (plasmacytoma), 228, 235f
Solitary osteochondromas, 208
Sonograms, 460
Spine
atlantoaxial subluxation, 300–301, 303f
infections, 433–434, 436f
metastases, 245, 247f
odontoid process, 300–301, 304f
osteoarthritis, 286, 290f
and sacroiliac joints, 310, 310f
thoracic and lumbar spine, 300
Spondylitis, 309
Spondyloarthritis (spondyloarthropathy)
ankylosing spondylitis, 304, 306
in lumbar spines, 306, 307f
sacroiliitis, 307, 308f
traumatic cervical spine fracture, 308, 308f
axial spondyloarthritis, 304–305
back pain, 306
biomechanical strength, 307
bony ankylosis, 307
differential diagnosis, 311, 311t
enteropathic spondyloarthropathy, 311, 311f
features, 304
orthopedic complication of, 307
peripheral polyarthritis, 307
psoriatic arthritis
feet, 309, 310f
HLA-B27, 309
inflammatory periostitis, 309, 310f
interdigitating erosions, 309, 309f
polyarthritis, 309
sacroiliitis and spondylitis, 309
“sausage digit” swelling, 309, 309f
spine and sacroiliac joints, 310, 310f
symmetric oligoarthritis, 309
symmetric seronegative polyarthritis, 309
reactive arthritis, 308–309, 309f
rheumatoid variants, 304
seronegative spondyloarthropathy, 304
subchondral granulation tissue, 306
syndesmophytes, 306, 307f
thoracolumbar/lumbosacral junctions, 306
Sports, thumb, 17–18
SPR (superior peroneal retinaculum), 178
STAR prosthesis, 362, 366f
Static stabilizers, 108
anterosuperior glenohumeral joint capsule, 114
Stener lesions, 171, 172f
Sternoclavicular joint, 32, 36f
STIR (short tau inversion recovery), 107
Stress fractures, 38, 147, 151f, 169
ankle
calcaneus, 183, 185f
of cuboid, 184, 187f
diaphyseal fractures, 184
of midfoot, 184, 187f
of navicular, 184, 186f
periosteal reaction, 184
of third metatarsal base, 184, 186f
of third metatarsal shaft, 184, 185f
of knee, 525f
of pelvis, 147, 150f
of pubic symphysis, 153, 158f
of sacrum, 147, 149f
thumb, 17–18
wrist arthroplasty, 382
Stress injuries
bony hypertrophy, 11
calcaneal stress fractures, 11–12, 11f
fatigue fractures, 11
insufficiency fractures, 11
muscular fatigue, 11
pathologic fractures, 11
periosteal edema, 11–12, 11f
second metatarsal stress fracture, 11–12, 12f
tibial stress fracture, 11f
Stromal bone formation, 243
Styloid process, 163
Subacromial-subdeltoid (SA-SD) bursa, 114, 116, 118f, 122, 124f
pathology, 123
Subchondral bone marrow edema, 297
Subchondral cyst formation, 278
Subchondral sclerosis, 523f
Subcoracoid bursa, 114
Subcutaneous calcifications, 302
Sublabral recess, 146, 147f
Subluxation, 278
Sub-scapularis bursa, 114
Subscapularis tendon, 114, 316, 318f
Subtalar joint, 331
Subtle labral tears, 107
Subtrochanteric fractures, 43–44, 46f–47f, 147
cantilevered configuration, 43
high-energy trauma, 43
insufficiency fracture, 44
pathologic fracture, 44
Subungual exostosis, 209–210
Sunburst periosteal reaction, 194, 196f, 504f
Superior glenohumeral ligament (SGHL), 108, 110f
Superior labrum anteroposterior (SLAP) labral tear, 109, 118, 121, 121f
Superior peroneal retinaculum (SPR), 178
Supra-acromial bursa, 114
Supracondylar process, 137, 138f
Suprapinatus muscle, 109
Supraspinatus tendon, 316, 318f
Symphalangism, 391, 392f
Syndactyly, 391, 392f
Syndesmophytes, 277, 306, 307f
Synovial chondromatosis, 322, 323f
Synovial chondrometaplasia, 322, 323f
Synovial cysts, 260, 322, 324f
Synovial fibrosis, 302
Synovial folds/plicae, 138, 139f
Synovial hyperemia, 296
Synovial hypertrophy, 277, 299
and effusion, 299
Synovial joints, 296
Synovial osteochondromatosis, 322, 323f
Synovial sarcoma, 256, 258f
Synovitis, acute, 316
Syphilis, 442
Syringomyelia, 314
Systemic and metabolic musculoskeletal conditions
acromegaly, 416, 417f
diabetes mellitus, 416, 417f
drug effects
antiepileptic drug–related bone disease, 422–423, 425f
bisphosphonates, 421, 423f
chemotherapeutic agents, 419
fluoride, 420–421, 421f
fluoroquinolone-associated tendinopathy, 422, 424f
highly active antiretroviral therapy (HAART), 423
methotrexate, 419
nephrogenic systemic fibrosis (NSF), 421–422, 424f
statins, 421
teratogenic effects, 419
vitamin A and analogues, 421, 422f
vitamin D toxicity, 419–420, 420f
hypercortisolism
muscle wasting, 416
nonendocrine adrenocorticotropic hormone–producing tumors, 415
osteonecrosis, 415–416
hypertrophic osteoarthropathy, 424, 426f
Paget disease (osteitis deformans)
in femur, 418, 419f
insufficiency fractures, 418, 419f
ivory vertebra, 418, 419f
at knee, 418, 418f
paramyxoviral infection, 417
in pelvis, 418, 420f
picture-frame vertebra appearance, 418, 418f
progression of, 417, 418f
trabecular appearance, 417
sarcoidosis, 423–424, 425f–426f
Systemic lupus erythematosus (SLE), 301–302, 305f, 511f
T
Talar dome osteochondral defect, 341, 341f
Talar osteotomy, 363
Talocalcaneal joints, 176
Talus
high-energy trauma, 52
lateral osteochondral fractures, 52
osteochondral defects, 52
Shepherd fracture, 52
subtalar dislocation, 52
Tarsal coalition, 337–338, 338f
Tarsal tunnel, 176, 178
Tarsometatarsal fracture-dislocation, 314
Tarsometatarsal (TMT) joint, 332
Telangiectatic osteosarcoma, 225, 229f
Tenosynovitis, 173
Tensile failure, avulsion injuries, 16, 17f
Teres minor muscle, 109
TFC (triangular fibrocartilage), 164, 165f, 168
TFCC (triangular fibrocartilage complex), 20, 168, 170, 171f
Palmer classification, 170, 171t
Thalassemia, 452–453, 454f, 520f
Therapeutic joint injections, 481
Thoracic cage
blunt chest trauma, 32
hyperflexion, 34
manubrium fracture, 34, 36f
rib fractures, 33, 36f
sternal body fracture, 37f
Thoracolumbar scoliosis, severe, 395, 395f
THRs (total hip replacements), 354, 355f
Thumb
abductor pollicis, 18
adductor pollicis, 18
avulsion fracture, 17–18, 18f
Bennett fracture, 18, 19f
carpometacarpal joint, 18
gamekeeper’s thumb, 17–18
ligamentous disruption, 17–18
metacarpophalangeal joint, 17–18
mobility, 18
Rolando fracture, 18, 19f
shallow saddle-shaped articulation, 18
ulnar collateral ligament rupture, 17–18
valgus stress, 17–18
violent hyperabduction, 17–18
Tibialis anterior tendon injuries, 179, 180f
Tibialis posterior muscle, 332
Tibialis posterior tendon, 331
Tibialis posterior tendon injuries, 178, 179f
Tibial plateau, 47
Tibial shaft, 47
transverse fracture, 494f
Time to echo (TE), 112
TMT (tarsometatarsal) joint, 332
Tophaceous gout
in carpus, 319, 320f
dual-energy CT (DECT), 319, 320f
in hand, 319, 320f
hyperuricemia, 319
in midfoot, 319, 320f
monosodium urate crystals, 319
overhanging edges and chronic erosions, 319, 320f
Total hip replacements (THRs), 354, 355f, 514f
Total knee replacement (TKR), 526f. See also Knee, surgery and replacement
Traction osteophyte, 277, 278f
Transcervical fractures, 146, 496f
Transient bone marrow edema syndrome, 149, 151f
Transverse humeral ligament, 114
Transverse intermeniscal ligament, 83, 86f
Trapezius muscle, 114
Trauma
bone biomechanics. See Bone biomechanics
burns/blast injuries. See Burns/blast injuries
fracture epidemiology, 1
fractures. See Fractures
open fractures. See Open fractures
posterior fat pad, 500f
soft-tissue biomechanics. See Soft-tissue biomechanics
soft-tissue injuries. See Soft-tissue injuries
stress injuries. See Stress injuries
Traumatic cervical spine fracture, 308, 308f
Traumatic injuries, 169
Triangular fibrocartilage complex (TFC), 164, 165f, 168
Triangular fibrocartilage complex (TFCC), 20, 170, 171f
Palmer classification, 170, 171t
Trochanteric bursa, 151, 154
Trochanteric bursitis, 469, 471f
Trochanteric pain syndrome, 151, 153f
Trochoginglymoid joint, 134
Tuberculosis, 434–435, 436f–438f
Tumoral calcinosis, primary, 262–263, 272f
Tumor reconstruction
bone graft substitute, 364, 368f
curettage, bone chips, 363–364, 367f
Doppler ultrasonography, 369
excisional resections, 364
graft failure, 366
massive intercalary tibial allograft, 366, 368f
methylmethacrylate cement, 364, 367f
oncologic bipolar hip replacement, 366, 368f
oncologic rotating hinge total knee replacement, 366, 369f
segmental resections, 365
Turf toe
plantar capsuloligamentous complex, 185, 189, 189f
from soccer injury, 189, 190f
Turret exostosis, 209
T1-weighted pulse sequences, 481
Type 2 lunate, 167, 167f
U
UBC (unicameral bone cyst), 217–218, 218f
Ulnar collateral ligament (UCL), 134–135, 135f, 139–140, 141f, 164
Ulnar impaction syndrome, 169, 170f, 502f
Ulnar variance, 168
Ulnocarpal ligaments, 164
Ulnohumeral articulation, 134
Ulnotriquetral and ulnolunate, 164
Ultrasound
accessory flat-panel screen, 460
anisotropy artifact, 460, 461f
ankle ultrasound, 472–474, 473f–476f
echogenicity of, 460
elbow, 463–465, 466f
fibroadipose tissue, 461
foot, 474, 477f
hand and finger, 467–468, 470f–471f
hematoma, 460
hip, 468–469, 471f–472f
hypoechoic abnormality, 460
knee, 469, 472, 473f
muscle fascicles, 461
rotator cuff barbotage, 486, 489f
shoulder
acromioclavicular joint, 462, 462f
biceps dislocation, 461, 462f
biceps tendon, 461, 461f
complete rotator cuff tear of, 462, 464f
infraspinatus tendon, 462, 464f
partial rotator cuff tear, 462, 463f
posterior glenohumeral joint, 462, 465f
spinoglenoid notch paralabral cyst, 463, 465f
subdeltoid-subacromial bursitis, 462–463, 465f
supraspinatus tendinosis, 462, 464f
supraspinatus tendon partial tear, 462, 464f
teres minor tendon, 462, 465f
sonograms, 460
tendinosis, 460
transducer, 521f
wrist
carpal tunnel, 466, 469f
de Quervain disease, 466, 468f
extensor carpi ulnaris (ECU) tendinosis, 466, 467f
extensor carpi ulnaris (ECU) tendon dislocation, 466, 467f
extensor pollicis longus (EPL) tendon rupture, 466, 468f
hardware impingement, 466, 469f
Ultrasound-guided injection, 479, 480f
Unicameral bone cyst (UBC), 217–218, 218f
Unrecognized soft-tissue injuries, 76
Upper extremity fractures
acromioclavicular joint (ACJ). See Acromioclavicular joint (ACJ)
carpal instability. See Carpal instability
clavicle. See Clavicle
distal radius. See Distal radius
elbow. See Elbow
fingers, 16–17
forearm. See Forearm
glenohumeral joint. See Glenohumeral joint, dislocations
humerus. See Humerus
isolated carpal bones. See Isolated carpal bones
perilunate injuries. See Perilunate injuries
scaphoid. See Scaphoid
sternoclavicular joint. See Sternoclavicular joint
thoracic cage. See Thoracic cage
thumb. See Thumb
wrist. See Wrist
V
Valgus stress, 138
Vascular bone lesions, 219, 219f
Vascular connective tissue stroma, 206
Vascularized fibular autograft, 350, 353f
Villonodular synovitis, 513f
Vitamin A, 421, 422f
Vitamin D
deficiency, 411–412, 412f
physiology and function, 410–411, 412f
toxicity, 419–420, 420f
Volar plate, 164, 166f
injury, 171, 172f
Volar ulnocarpal ligaments, 164
W
Wires and cables
ankle syndesmosis, 69, 70f
cerclage wires, 68, 69f
flexible fixation, 69, 69f
Kirschner wires (K-wires), 68, 68f
tension bands, 68, 68f
World Health Organization classification, 255
Wrisberg ligament, 83
Wrisberg rips, 88, 90f
Wrist, 522f
arthroplasty
carpal arthrodesis, 377, 380f
conditions, 375
distal radioulnar joint (DRUJ), 377–378, 381f
four-corner fusion, 376, 379f
gadolinium-based contrast, 378
proximal row carpectomy, 376, 379f
Scheker prosthesis, 378
total radiocarpal arthroplasty, 376, 380f
triangular fibrocartilage, 378
ulnar head replacement hemiarthroplasty, 378, 381f
dorsal ligaments, 20
flexion and extension, 19
injection, 482–483, 485f
injuries
abduction stress, UCL, 170
abductor pollicis longus (ABPL) tendon, 168
accessory adductor digiti minimi, 168, 168f
adductor aponeurosis, 171
annular pulley tear, 172, 173f
bifid median nerve, 168, 169f
boutonniere injury, 173, 174f
carpal boss, 168, 168f
carpal osseous anatomy, 163, 164f
carpal tunnel, 164, 166, 167f, 174
chronic stenosing tenosynovitis, 173
classifications, 169
collateral ligament injuries, 170
collateral ligaments, 164, 166f
de Quervain syndrome, 172, 173f
distal interphalangeal (DIP) joints, 164
distal radioulnar joint (DRUJ), 163
dorsal extrinsic ligaments, 164
dorsal intercalated segment instability, 169
extensor carpi ulnaris (ECU), 163, 173, 173f
extensor hood mechanism, 172
extensor tendons, 164, 167f
extrinsic ligaments, 164, 166f
fibrocartilaginous structure, 164
fibro-osseous tunnel, 166
flexor tendons, 164, 166, 167f, 172
Guyon’s canal, 166, 174
handlebar palsy, 174
hood apparatus, 164
intersection syndrome, 172
intrinsic carpal ligaments, 164
intrinsic ligament injury, 170, 171f
jersey finger, 173, 174f
long radiolunate, 164
lunate and triquetrum, 164, 165f
lunotriquetral coalition, 167, 167f
lunotriquetral ligaments, 164, 165f, 170
mallet finger, 173, 174f
median neuropathy, 174, 174f
metacarpophalangeal (MCP) joint, 164
midcarpal joint, 163
osseous structures, 164
overuse injuries, 169
peritendinitis, 173
progressive osteoarthritis, 169–170
proximal interphalangeal (PIP) joint, 164
pulse sequence, 163
radiocarpal joint, 163
radiocarpal ligaments, 164
radioscaphocapitate, 164
radioulnar ligaments, 164, 165f
sagittal band rupture, 172, 172f
scaphoid fractures, 169, 169f, 495f, 502f
scapholunate advanced collapse wrist, 170, 171f, 512f
scapholunate ligaments, 164, 165f, 169
short radiolunate, 164
Stener lesions, 171, 172f
styloid process, 163
tenosynovitis, 173
traumatic injuries, 169
triangular fibrocartilage complex (TFC), 164, 165f , 168
triangular fibrocartilage complex (TFCC) tear, 170, 171f, 171t
type 2 lunate, 167, 167f
ulnar collateral ligament (UCL), 164
ulnar impaction syndrome, 169, 170f
ulnar variance, 168
ulnocarpal ligaments, 164
ulnotriquetral and ulnolunate, 164
volar plate, 164, 166f, 171, 172f
volar ulnocarpal ligaments, 164
instability, 20
interosseous ligaments, 20
ligaments, 19f, 20
lunate, 19
radiographic evaluation, 20
range of motion, 19
rheumatoid arthritis (RA), 296, 298, 300f
with tenosynovitis, 298, 301f
scaphoid, 19–20
space of Poirier, 20
triangular fibrocartilage complex (TFCC), 20
triquetrum, 19–20
ultrasound
carpal tunnel, 466, 469f
de Quervain disease, 466, 468f
extensor carpi ulnaris (ECU) tendinosis, 466, 467f
extensor carpi ulnaris (ECU) tendon dislocation, 466, 467f
extensor pollicis longus (EPL) tendon rupture, 466, 468f
hardware impingement, 466, 469f
volar carpal ligaments, 20

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Musculoskeletal

Copyright © 2019 Felix S. Chew.

Library of Congress Cataloging-in-Publication Data

Names: Chew, Felix S., editor.

This work is no substitute for individual patient assessment based upon

Given continuous, rapid advances in medical science and health information,

Kimia Khalatbari Kani, MD

he Essentials series is a collection of radiology textbooks following a

JANNETTE COLLINS, MD, MED, FCCP, FACR

Chapter 1 Imaging Basics of Musculoskeletal Trauma

Chapter 2 Imaging of Upper Extremity Fractures and Dislocations

Chapter 3 Imaging of Lower Extremity Fractures and Dislocations

Chapter 4 Imaging of Fracture Treatment and Healing

Chapter 5 MRI of Knee Injuries

Chapter 6 MRI of Shoulder Injuries

Chapter 7 MRI of Elbow Injuries

Chapter 8 MRI of Hip Injuries

Chapter 9 MRI of Wrist and Hand Injuries

Chapter 10 MRI of Ankle and Foot Injuries

Chapter 11 Imaging Basics of Bone Tumors

Chapter 12 Imaging of Benign Bone Lesions

Chapter 13 Imaging of Malignant Bone Tumors

Chapter 14 Imaging of Musculoskeletal Metastases

Chapter 15 Imaging of Soft-Tissue Lesions and Calcifications

Chapter 16 Imaging Basics of Arthritis

Chapter 17 Imaging of Osteoarthritis

Chapter 18 Imaging of Inflammatory Arthritis

Chapter 19 Noninflammatory Joint Disease

Chapter 20 Imaging of Nontraumatic Foot Conditions

Chapter 21 Imaging of the Postsurgical Lower Extremity

Chapter 22 Imaging of the Postsurgical Upper Extremity

Chapter 24 Osteoporosis and Abnormal Mineral Metabolism

Chapter 25 Imaging of Systemic and Metabolic Musculoskeletal

Chapter 26 Imaging of Musculoskeletal Infections

Chapter 27 Imaging of Bone Marrow Conditions

Chapter 28 Musculoskeletal Ultrasound

Chapter 29 Procedures in Musculoskeletal Radiology

Trauma is the reason most radiographs of the musculoskeletal system are

Force and Deformation

Bone is a diphasic material composed of a rigid calcium hydroxyapatite

Loading and Fractures

Traction or tension fractures result from traction on a bone by a tendon or

Longitudinal compressive loading of the shaft of a long bone results in an

Many fractures are produced by a combination of forces. Angulation with

On radiographs, fractures of cortical bone are definitively recognized as focal

On radionuclide bone scans, fractures are evident as regions of focal

Table 1.1 GRADING OF SPRAINS AND STRAINS

On radiographs, injuries of ligaments and joint capsules (sprains) and of

On sonography, the appearance of normal ligaments, tendons, and muscles,

FIGURE 1.20 • Open, comminuted fracture-dislocation of the ankle. Lateral

Low-velocity gunshot wounds are caused by pistols and many small-bore

BURNS AND BLAST INJURIES

The morphology of the fracture should be described in terms of the principal

Alignment refers to the long axis of the fragments; angulation is a change

Position refers to the relationship of the fracture fragments to their normal

CHAPTER SELF-ASSESSMENT QUESTIONS

1. Avulsion fractures typically result from which form of biomechanical loading?

2. Which 2 demographic groups have the highest incidence of fractures?

3. Bayonet apposition is a descriptive term that may be most appropriately

4. Which biomechanical mechanism of fracture typically results in comminution?

Answers to Chapter Self-assessment Questions

Table 2.1 PERILUNATE INJURIES OF THE WRIST

DISTAL RADIUS AND FOREARM