Tải bản đầy đủ (.pdf) (100 trang)

Skeletal imaging, atlas of the spine and extremities 2nd ed j taylor, t hughes, d resnick (saunders, 2010) 1

Bạn đang xem bản rút gọn của tài liệu. Xem và tải ngay bản đầy đủ của tài liệu tại đây (3.89 MB, 100 trang )


3251 Riverport Lane
Maryland Heights, Missouri 63043

SKELETAL IMAGING: ATLAS OF THE SPINE AND EXTREMITIES,
SECOND EDITION

ISBN 978-1-4160-5623-2

Copyright © 2010, 2000 by Saunders, an imprint of Elsevier Inc.
All rights reserved. No part of this publication may be reproduced or transmitted in any form or by
any means, electronic or mechanical, including photocopying, recording, or any information storage
and retrieval system, without permission in writing from the publisher. Permissions may be sought
directly from Elsevier’s Rights Department: phone: (+1) 215 239 3804 (US) or (+44) 1865 843830
(UK); fax: (+44) 1865 853333; e-mail: You may also complete your
request on-line via the Elsevier website at />
Notice
Neither the Publisher nor the Authors assume any responsibility for any loss or injury and/or
damage to persons or property arising out of or related to any use of the material contained in
this book. It is the responsibility of the treating practitioner, relying on independent expertise and
knowledge of the patient, to determine the best treatment and method of application for the
patient.
The Publisher
Library of Congress Control Number: 2009935763

Vice President and Publisher: Linda Duncan
Senior Acquisitions Editor: Kellie White
Associate Developmental Editor: Kelly Milford
Publishing Services Manager: Catherine Jackson
Senior Project Manager: Karen M. Rehwinkel
Design Direction: Jessica Williams



Working together to grow
libraries in developing countries
www.elsevier.com | www.bookaid.org | www.sabre.org

Printed in the United States of America
Last digit is the print number:

9

8

7

6

5

4

3

2

1






To my parents and siblings,
who taught me the importance of hard work and persistence;
to my mentors who taught me the importance of lifelong learning;
to my students who provide continuous motivation;
and to my co-authors, Tudor Hughes and Donald Resnick.
JAMT
To my coauthor, John, who is clearly the first author.
And to my always-supportive family: my loving wife Kelly;
my three wonderful boys, Geraint, Griffith, and Rhett;
and my learned parents, Dorothy and Fred.
THH
It was a great pleasure and a distinct honor for me to work with two
skilled colleagues and friends, John Taylor and Tudor Hughes,
whose efforts far overshadow my contributions to this text.
They brought organization, dedication, and enthusiasm to
the project, sprinkled with good old-fashioned energy.
DR

v



PREFACE
BACKGROUND
We initially intended the Second Edition of Skeletal
Imaging to be merely a modification of the First Edition.
We planned only on updating the original and adding
new case material that illustrates the more recent
advances in the imaging diagnosis of musculoskeletal
disorders. After all, only 9 years had elapsed between

publication of the first edition, and the beginning of
research for this edition. However, our survey of the
literature published since 2000 persuaded us that a
wealth of new information deserved synthesis and
recognition. Our major dilemma was not so much to
decide what to include, but what to exclude, and still
meet our two principal objectives—to limit the atlas to
a single volume and to address the most important musculoskeletal disorders. Accordingly, we have focused on
disorders most frequently encountered in practice and on
how those disorders appear on conventional radiography, CT scans, MR images, and to a lesser extent, radionuclide imaging and diagnostic ultrasonography.

WHO WILL BENEFIT FROM THIS BOOK?
Radiologists, chiropractors, and other clinicians who
routinely interpret images of the musculoskeletal system
will find the second edition an indispensable everyday
reference. Radiology residents, chiropractic students,
and other clinicians-in-training who are preparing for
certification examinations can use it in the classroom, at
the viewbox or monitor, and as a helpful study guide.

ORGANIZATION
The second edition retains the same organizational strategy: arranging musculoskeletal disorders according to
anatomic region. This organization enhances the book’s
value as a reference tool for practitioners and is a practical way for students to learn a logical and methodical
approach to patient assessment. Each chapter includes a
description of the appearance of normal developmental
anatomy and major anomalies and anatomic variants. It
also demonstrates the full range of the most frequently
encountered pathologic conditions, including dysplasias,
physical injuries, internal derangements of joints, articular disorders, and bone tumors, as well as metabolic,

hematologic, and infectious diseases.
Specifically, Chapter 1, “Introduction to Skeletal Disorders: General Concepts,” consists of 19 tables summarizing the general characteristics of the most common
disorders discussed and illustrated throughout the text.
These tables offer an overview of information, such as

age of onset, sites of involvement, clinical features, and
general imaging features. This chapter was developed to
avoid repetition of background material about disorders
that affect several anatomic regions. Chapters 2 to 17
represent stand-alone monographs, each dealing with a
specific anatomic site. The tables in these chapters
emphasize only the site-specific manifestations of each
entity, and they provide a sense of the range of disorders
that characteristically affect that site. Furthermore, in
each of these regional chapters, most of the important
conditions are illustrated with routine radiographs, some
of which are supplemented with conventional tomograms, CT or bone scans, MR images, or combinations
of these. In addition, the chapters dealing with spinal
regions and joints contain tables and illustrations of the
normal developmental anatomy of that region through
infancy, childhood, and adolescence. When reading these
chapters, it may be useful, or even necessary, to refer to
Chapter 1 for a more detailed discussion of the general
features of a particular disorder.
The major emphasis of this work, however, is on the
illustrations that the authors believe represent the most
characteristic or typical presentations of disease entities.
For the most part, the cases include commonly encountered disorders, although some disorders that are seen
less commonly also are included because they are important to consider with regard to differential diagnosis.
Purposely, the illustrations are as large as possible to best

display the imaging findings. Each is accompanied by a
detailed legend beginning with the primary diagnosis
followed by a discussion of the imaging findings and any
available and important clinical data. When MR imaging
is displayed, detailed imaging parameters are included in
the legend.
At least one useful reference for each condition has
been included. The references are cited not only in the
tables but also in the figure legends. These reference citations indicate the major sources of material and serve to
direct the reader to further discussion. In Chapter 1, a
bibliography of recommended readings includes many
textbooks dealing with various aspects of skeletal radiology that served as sources for information.
It is our hope that by retaining the successful features
and format of the First Edition, updating the text to
reflect new information, and adding more case material
that this edition will be as favorably received by readers
and reviewers.
John A. M. Taylor
Tudor H. Hughes
Donald Resnick

vii



ACKNOWLEDGMENTS
For the Second Edition
Many colleagues and friends who generously contributed so much to the first edition have done so again, in
a variety of ways, for this revised second edition of
Skeletal Imaging. We are enormously indebted to Dr.

Brian Howard for contributing many more excellent case
studies from his teaching files; to Stephanie Brown, DC,
for compiling research material in the formative stages
of revision; and to Gary Smith, DC, DACBR, Matthew
Richardson, DC, and Laurie Rocco, DC, for carefully
and thoroughly proofreading every chapter, word by
word. We thank Pete Broomhall for editorial advice and
assistance and Karen Rehwinkel and the other professionals of the Elsevier team and Saunders for providing
encouragement, advice, and assistance at every turn. We
are particularly indebted to our editors, Kellie White and
Kelly Milford, for patiently and gently guiding us through
every stage of production and for attempting to keep us
on task and on schedule.

The original two authors of Skeletal Imaging are enormously indebted to Dr. Tudor Hughes, a well-respected
musculoskeletal radiologist and educator at the University of California, San Diego, and the second edition’s
recently recruited third author. His extensive knowledge
and understanding of musculoskeletal disorders is
matched by equally impressive skills in researching, factchecking, writing, and editing. In addition to contributing hundreds of fascinating cases from his vast digital
teaching files, he improved every chapter of Skeletal
Imaging by making them more accessible to and productive for the reader.
John A. M. Taylor
Donald Resnick

John A. M. Taylor
Tudor H. Hughes
Donald Resnick

ix



ACKNOWLEDGMENTS
For the First Edition
The authors wish to acknowledge their appreciation of
several persons who have generously contributed their
time, effort, and case material during the production of
this text. First, as is indicated in the legends associated
with the illustrations, approximately 140 colleagues
contributed one or more cases for inclusion in this atlas.
Their willingness to share case material with us is very
much appreciated. Of these persons, many deserve
special mention for their donation of several cases: Drs.
John Amberg, Appa Anderson, Richard Arkless, Felix
Bauer, Gabrielle Bergman, Eve Bonic, Enrique Bosch,
Sevil Kursunoglu Brahme, Thomas Broderick, Ann
Brower, Clement Chen, Armando D’Abreu, Larry
Danzig, Steven Eilenberg, Douglas Goodwin, Guerdon
Greenway, Jorg Haller, Al Nemcek, Beverly Harger,
Brian Howard, Roger Kerr, Phillipe Kindynis, Michael
Mitchell, Arthur Newberg, Mini Pathria, Carlos Pineda,
Jean Schils, Jack Slivka, Gary Smith, Richard Stiles,
Phillip VanderStoep, Christopher Van Lom, and Vinton
Vint. Numerous radiographs illustrating normal
developmental anatomy were donated by Dr. David
Sartoris from the University of California, San Diego;
Dr. Jeffrey Cooley from Los Angeles College of
Chiropractic; and Dr. Beverly Harger from Western

x


States Chiropractic College. The authors also wish to
acknowledge a number of persons who have willingly
proofread portions of the manuscript at various stages
of completion: Bill Adams, Eve Bonic, Todd Knudsen,
Chad Warshel, Peter Broomhall, and especially Gary
Smith, who was kind enough to carefully read and
re-read every chapter.
The atlas would not have been possible without the
input of a team of professionals at WB Saunders: Lisette
Bralow, Frank Polizzano, Mary Reinwald, Walt
Verbitski, Nicholas Rook, and Nancy Matthews. Their
expertise and advice were crucial to the production of
the atlas.
Finally, two members of our team who from the
outset were absolutely essential to the completion of the
text deserve recognition for their extraordinary efforts.
Debra Trudell, our technical assistant, produced the
photographic reproductions. Catherine Fix, our copy
editor, meticulously edited every table, caption, and
reference throughout the text. Their expertise, attention
to detail, and demand for excellence are evident
throughout the atlas. The authors are deeply indebted to
Debra and Catherine and, indeed, to all of the persons
cited here.


PA R T

I
Introduction


CHAPTER

1

Introduction to Skeletal Disorders: General Concepts

Many bone and joint disorders affect multiple regions of
the skeleton. The tables in this chapter list anomalies and
anatomic variants (Table 1-1), skeletal dysplasias (Table
1-2), spinal dysraphisms (Table 1-3), fractures (Tables
1-4 and 1-5), articular injuries (Table 1-6), articular
disorders (Tables 1-7 to 1-11), bone tumors (Tables 1-12
and 1-13), tumorlike lesions of bone (Table 1-14), metabolic, nutritional, and endocrine disorders (Table 1-15),
hematologic disorders (Table 1-16), osteonecrosis (Table

1-17), osteochondroses (Table 1-18), and infectious disorders of bones and joints (Table 1-19). These tables are
intended to provide the reader with an overview of the
common clinical, laboratory, and radiographic features
of the more common disorders that typically appear in
more than one skeletal location. Site-specific findings and
features unique to each anatomic region are discussed
further in subsequent chapters.

1


CHAPTER 1

2


TAB L E 1- 1

Introduction to Skeletal Disorders: General Concepts

Developmental Anomalies, Anatomic Variants, and Sources of Diagnostic Error: Concepts
and Terminology*
Examples

Entity

Characteristics

Terminology

Spine

Extremities

Developmental
anomaly

Marked deviation from normal standards as a
result of a congenital or hereditary defect;
such malformations usually represent a
primary problem in the morphogenesis
of a tissue
May be asymptomatic or associated with
significant clinical manifestations
Spinal anomalies—general concepts:

1. Most spinal anomalies occur at transitional
areas, such as the craniocervical,
cervicothoracic, and thoracolumbar regions
2. When one anomaly is identified, always
search for more because anomalies may
be multiple
3. Anomalies may be isolated or associated
with a syndrome
4. Osseous anomalies may be associated with
underlying neurologic or visceral anomalies

Nonsegmentation or
synostosis
Aplasia or agenesis
Hypoplasia

Block vertebrae

Tarsal coalition

Odontoid agenesis
Hypoplastic C1
posterior arch
Transverse process
hyperplasia
Transitional segments

Radial aplasia
Glenoid hypoplasia


A modification of some anatomic
characteristic that is considered normal
Usually not associated with clinical
manifestations; often encountered as an
incidental finding

Areas of normal
trabecular
diminution or
prominence
Normal sites of
osseous
irregularity

Prominent Hahn
venous channels

Humeral pseudocyst
Ward triangle of femur
Pseudocystic region of
calcaneus
Avulsive cortical
irregularity of the
femur

Misdiagnosis may occur under various
conditions:
Normal structures may be interpreted as
abnormal owing to overlying shadows
created by gas, soft tissue, or

malpositioned structures
Rarefactions, irregularities, depressions, or
proliferations of bone may be mistaken for
evidence of disease

Overlying normal
anatomy

Mach effect overlying
odontoid,
simulating fracture

Quadriceps muscle plane
overlying femur,
simulating fracture

Anatomic irregularities

Normal notch in
superior
articulating
process, simulating
cervical pillar
fracture
Osteosclerotic anterior
arch of atlas,
simulating an
osteoblastic lesion

Normal sclerosis and

fragmentation of
calcaneal apophysis,
simulating
osteochondrosis

Anatomic
variant

Sources of
diagnostic
error

Slight modifications in osseous anatomy may
be judged to be significant

Hyperplasia
Supernumerary bones

Anatomic variants

Cupid bow
configuration of
vertebral body
simulating
endplate fracture
or Schmorl nodes

Focal gigantism
Polydactyly


Rhomboid fossa in
clavicle, simulating a
destructive lesion

Data from Jones K: Smith’s recognizable patterns of human malformation. 6th ed. Philadelphia, Saunders, 2005.
* The differentiation of anomalies, anatomic variants, and sources of error is often indistinct, owing to considerable overlap in the definitions.


CHAPTER 1
TAB L E 1- 2

Introduction to Skeletal Disorders: General Concepts

3

Skeletal Dysplasias and Other Congenital Disorders

Entity

General Characteristics

General Imaging Findings

Achondroplasia

Relatively common rhizomelic dwarfism
Accentuated lumbar lordosis, waddling gait, prominent
forehead, depressed nasal bridge, trident hand
Short proximal extremities, normal length of spine
Complications

Spinal stenosis
Brain stem compression from narrow foramen magnum

Spinal stenosis with posterior scalloping of vertebral
bodies and decreased spinal canal diameter
Vertebral bodies may be flattened or wedge-shaped
Diaphyseal widening of long bones
Narrow thorax, champagne glass pelvis
Splayed and cupped metaphyses of long bones

Diastrophic dysplasia

Rare autosomal recessive dwarfing dysplasia

Short stature, progressive scoliosis, kyphosis

Spondyloepiphyseal
dysplasia

Congenita form
Autosomal recessive, rhizomelic dwarfism
Short trunk, respiratory and visual complications

Congenita form
Decreased height of vertebral bodies, pear-shaped
vertebrae in childhood, kyphoscoliosis, accentuated
kyphosis and lordosis, pectus carinatum, delayed
ossification, hypoplasia of the odontoid with
atlantoaxial instability
Tarda form

Heaped-up vertebrae, platyspondyly, disc space narrowing

Tarda form
Milder, X-linked recessive form seen only in males
Rare lethal form
Also termed hypochondrogenesis
Dysplasia epiphysealis
hemimelica

Trevor disease
Uncommon developmental disorder
Asymmetric cartilaginous overgrowth in one or more
epiphyses
May be localized or generalized
Joint dysfunction, pain, limitation of motion, and a mass
may accompany the disease

Mucopolysaccharidoses Enzyme deficiencies result in radiographic changes
(MPS)
termed dysostosis multiplex
Two types most commonly encountered: Hurler and
Morquio syndromes

Resembles large eccentric osteochondroma arising from
epiphyses particularly about the knee and ankle
Bulky irregular ossification extending into soft tissues
Computed tomographic (CT) or MR imaging may be
useful to show the exact location and extent of the
lesion and the presence of joint involvement


MPS I-H (Hurler syndrome)
Atlantoaxial instability may be present
Rounded anterior vertebral margins with inferior beaking
Posterior scalloping of vertebral bodies
Paddle ribs, flared ilia, coxa valga, and coxa vara
deformities
MPS IV (Morquio syndrome)
Hypoplastic or absent odontoid process with atlantoaxial
instability
Flattened vertebral bodies (platyspondyly)
Posterior scalloping of vertebral bodies
Short, thick tubular bones

Fibrodysplasia
ossificans
progressiva

Rare autosomal dominant disease
Progressive ossification of skeletal muscle
Results in limitation of motion, weakness, and eventual
respiratory failure

Sheetlike ossification within soft tissues of neck, trunk,
and extremities
Hypoplastic vertebral bodies and intervertebral discs
Apophyseal joint ankylosis
Shortening of thumbs and great toes

Cleidocranial dysplasia


Rare autosomal dominant disorder characterized by
incomplete ossification
Widened cranial vault
Drooping shoulders
Abnormal gait, scoliosis, hypermobility, and dislocations
of shoulders and hips
Deafness, severe dental caries, and infrequently, basilar
impression

Absent or hypoplastic clavicles
Spine: multiple midline defects of the neural arch (spina
bifida)
Pelvis: widened symphysis pubis, coxa valga, coxa vara,
underdeveloped bones with small pelvic bowl
Skull: wormian bones, persistent metopic suture

Osteopetrosis

Sclerosing dysplasia
Benign (autosomal dominant), intermediate, and lethal
(malignant autosomal recessive) forms
Complications: anemia, osteomyelitis, blindness,
deafness, hemorrhage; brittle bones predispose to
bone fragility and pathologic fracture

Patterns of osteosclerosis: diffuse osteosclerosis,
bone-within-bone appearance, sandwich vertebrae

Continued



TAB L E 1- 2

Skeletal Dysplasias and Other Congenital Disorders—cont’d

Entity

General Characteristics

General Imaging Findings

Osteopoikilosis

Asymptomatic sclerosing dysplasia
No associated complications

Multiple 2- to 3-mm circular foci of osteosclerosis
Symmetric periarticular lesions resembling bone islands
predominate about the hip, shoulder, and knee

Osteopathia striata

Extremely rare asymptomatic sclerosing dysplasia
No associated complications

Regular, linear, vertically oriented bands of osteosclerosis
extending from the metaphysis for variable distances
into the diaphysis
Metaphyseal flaring also may be seen
May be related to cranial sclerosis and focal dermal

hypoplasia (Goltz syndrome)

Melorheostosis

Rare sclerosing dysplasia
Clinical findings
May be associated with intermittent joint swelling, pain
and limitation of motion, muscle contractures,
tendon and ligament shortening, growth
disturbances in affected limbs, and other
musculoskeletal abnormalities

Usual pattern: hemimelic involvement of a single limb
Peripherally located cortical hyperostosis resembling
flowing candle wax on the surface of bones
Para-articular soft tissue calcification and ossification may
occur and may even lead to joint ankylosis
May be positive on bone scans

Mixed sclerosing bone
dystrophy

Rare condition in which patients have radiologic
findings characteristic of more than one, and
occasionally all, of the sclerosing dysplasias

Combinations of osteopetrosis, osteopoikilosis,
osteopathia striata, and melorheostosis

Chondrodysplasia

punctata

Conradi-Hünermann syndrome or stippled epiphyses
Several different types of this rare multiple epiphyseal
dysplasia have been identified, including mild and
lethal forms
Mild dwarfism, mental retardation, and joint
contractures

Stippled calcification of vertebral bodies and epiphyses
of the extremities
In the rhizomelic form, coronal clefts are present within
the vertebral bodies

Osteogenesis
imperfecta

Inherited connective tissue syndrome
Type II, congenital lethal form, has a high infant
mortality rate
Type I, the more common form, exhibits milder changes
and is associated with a normal life expectancy
Associated with osteoporosis and bone fragility, various
degrees of dwarfism, blue sclera, ligament laxity,
dentinogenesis imperfecta, and premature
otosclerosis
Complicated by multiple fractures, deafness, and
pneumonia

Severe osteoporosis

Pencil-thin cortices
Multiple fractures of vertebrae and long bones
Bowing deformities of long bones, especially lower
extremity
Rare cystic form—ballooning of bone, metaphyseal
flaring, and honeycombed appearance of thick
trabeculae

Progressive diaphyseal
dysplasia

Rare autosomal dominant disorder also termed
Camurati-Engelmann disease
Typically bilateral and confined to the diaphyseal region
of bone
Progressive diaphyseal dysplasia affects predominantly
the lower extremity
Usually self-limited, resolving by 30-35 years of age

Bilateral fusiform thickening of the diaphysis of the long
bones
Cortical thickening and hyperostosis result in increased
diaphyseal radiodensity

Hereditary osteoonychodysostosis
syndrome

Also termed Fong syndrome, HOOD syndrome, and
nail-patella syndrome
Associated with abnormalities of the fingernails and

toenails

Absent or hypoplastic patellae
Patellar dislocation, iliac horns, and radial head
dislocation

Marfan syndrome

Autosomal dominant connective tissue disorder
Muscular hypoplasia, joint laxity, dislocations, cataracts
Complications: aortic aneurysm, lens dislocation

Long slender bones, arachnodactyly, thin cortices
Kyphoscoliosis in 40%-60% of persons
Posterior vertebral body scalloping from dural ectasia
Significant osteopenia independent from body mass index
(BMI)

Ehlers-Danlos
syndrome

Rare connective tissue disorder characterized by joint
hypermobility, blood vessel fragility, and skin
elasticity; many forms identified
Complications: valvular insufficiency, aortic aneurysm
and dissection

Posterior scalloping of vertebral bodies
Platyspondyly and kyphoscoliosis
Genu recurvatum and other joint subluxations

Heterotopic myositis ossificans
Subcutaneous hemangiomas (calcified phleboliths)

For more detailed discussion, refer to:
Murray RO: The radiology of skeletal disorders. 3rd ed. New York, Churchill Livingstone, 1989.
Taybi H, Lachman RS: Radiology of syndromes, metabolic disorders, and skeletal dysplasias. 5th ed. St Louis, Mosby-Year Book, 2007.
Yochum TR, Rowe LJ: Essentials of skeletal radiology. 3rd ed. Baltimore, Williams & Wilkins, 2004.


CHAPTER 1

TAB L E 1- 3

Introduction to Skeletal Disorders: General Concepts

5

Classification of Spinal Dysraphisms*

Entity

Description

Open spinal dysraphisms
• Myelomeningocele
• Myelocele
• Hemimyelomeningocele
• Hemimyelocele

In open spinal dysraphisms, nervous tissue is exposed to the

environment

Closed spinal dysraphisms

Closed spinal dysraphisms are covered by skin and therefore are
not exposed to the environment
50% have cutaneous birth marks

With subcutaneous mass—lumbosacral
• Lipomas with dural defect: lipomyelomeningocele and lipomyelocele
• Terminal myelocystocele
• Meningocele
With subcutaneous mass—cervicothoracic
• Nonterminal myelocystocele
• Meningocele
Without subcutaneous mass—simple dysraphic states
• Intradural lipoma
• Filar lipoma
• Tight filum terminale
• Persistent terminal ventricle
• Dermal sinus
Without subcutaneous mass—complex dysraphic states
• Disorders of midline notochordal integration
a. Dorsal enteric fistula
b. Neurenteric cysts
c. Diastematomyelia
• Disorders of notochordal formation
a. Caudal agenesis
b. Segmental spinal dysgenesis
* Modified from Rossi A, Gandolfo C, Morana G, et al: Current classification and imaging of congenital spinal abnormalities. Semin Roentgenol 41:250, 2006.



Sites of skeletal metastasis, simple bone cyst,
enchondroma, giant cell tumor, plasma cell
myeloma, lymphoma, Ewing sarcoma, and
other large osteolytic or osteosclerotic
lesions
Pars interarticularis of lumbar vertebrae
(spondylolysis), metatarsal bones in military
recruits (march fracture), and the lower
extremity in athletes, joggers, and dancers
Sacrum, pubic rami, and lower extremity about
the ankle, foot, knee, and hip

Fatigue fracture

Insufficiency fracture

Pathologic fractures

Stress-related bone
injuries*

Tibial plateau
Vertebral body

Fracture resulting from repeated cyclic loading applied to normal bones, with the load being
less than that which causes acute fracture of bone
Athletic, recreational, and occupational injuries are most common causes
Tibial or femoral fatigue fractures may be longitudinal, involving a major portion of the

diaphysis
Pathologic fracture through a bone weakened by a disease process, initiated with forces
insufficient to fracture a normal bone
Disease processes include rheumatoid arthritis, osteoporosis, Paget disease, osteomalacia or
rickets, hyperparathyroidism, renal osteodystrophy, osteogenesis imperfecta, osteopetrosis,
fibrous dysplasia, and irradiation
High signal intensity on T2-weighted and low signal intensity on T1-weighted spin echo MR
sequences; scintigraphy also positive

Fracture through a bone weakened by a disease process (such as osteoporosis, neoplasm,
infection, or metabolic disease) with forces insufficient to fracture a normal bone
Insufficiency fracture is a term commonly applied to pathologic fractures occurring at sites of
nontumorous lesions (see stress-related bone injuries)

One hard bone surface is driven into an apposing softer bone surface
Forceful flexion of the spine resulting in a wedge fracture of the vertebral body with depression
of the endplate within the spongiosa bone of the vertebral body

Any bone
Most fractures are closed
Any bone, especially long, tubular bones
Femoral and humeral diaphyses
Femur, rib (flail chest)

Closed fracture
Comminuted
fracture
Butterfly fragment
Segmental fracture


Depression fracture
Compression
fracture

Any site, particularly femur, tibia, and humerus

Open fracture

CHAPTER 1

Impaction fractures

Imaging findings
Soft tissue defect, bone protruding beyond soft tissues, subcutaneous or intraarticular gas,
foreign material beneath skin, absent pieces of bone
Associated with high-impact trauma; high rate of infection
Simple fracture in which the bone does not break through the skin
Fracture with more than two fracture fragments
Associated with high-impact injuries and crush injuries
Wedge-shaped fragment arising from the shaft of a tubular bone at the apex of the force input
Fracture lines isolate a segment of the shaft of a tubular bone

Any tubular bone

Position

Any tubular bone, particularly lower extremity

Alignment


Characteristics

Transverse: bending or angular forces in long bones; tensile or traction forces in short bones;
also pathologic fracture such as occurs with tumors
Oblique: compression, bending, and torsion forces
Oblique-transverse: combination of axial compression and bending forces
Spiral: torsion forces
Varus angulation: angulation of the distal fragment toward the midline of the body
Valgus angulation: angulation of the distal fragment away from the midline of the body
Anterior or posterior angulation: anterior or posterior angulation of the distal fragment
Relationship of fracture fragments, exclusive of angulation: displaced or undisplaced fractures
Displacement: abnormalities of apposition and rotation
Apposition: degree of bone contact at the fracture site: undisplaced fractures have 100%
apposition; fracture surfaces may be separated and are termed distracted fractures;
overlapping of fracture surfaces with consequent shortening is termed a bayonet deformity
Rotation: rotation about the longitudinal axis; difficult to assess from routine radiographs
Communication between fracture and outside environment because of disruption of the skin

Any tubular bone

Orientation

Acute fractures

Typical Sites of Involvement

Classification

Fractures in Adults: Concepts and Terminology


Entity

TABLE 1-4

6

Introduction to Skeletal Disorders: General Concepts


Fracture of cartilage alone: chondral fracture
Fracture of bone and cartilage: osteochondral fracture
Shearing, rotational, or tangentially aligned impaction forces generated by abnormal joint
motion may result in fractures of two apposing joint surfaces
Momentary, persistent, or recurrent dislocations and subluxations may result in these injuries
Associated with painful joint effusion, joint locking, clicking, and limitation of motion;
intraarticular bodies common; bodies may attach to synovium and eventually resorb

Distal portion of femur, patella, humeral head,
glenoid rim, elbow, or hip

Femoral condyles and talus are most typical
sites
Less common sites: other tarsal bones, tibia,
humeral head, glenoid cavity, acetabulum,
and elbow (capitulum)
Patellar involvement is rare

Tibial tubercle, olecranon, pelvis, hip, tibial
eminence, spinous process
Scaphoid and improperly immobilized fracture

sites
Scaphoid, femoral neck, tibia, clavicle,
odontoid process (os odontoideum), or any
site improperly immobilized
Also occurs in neurofibromatosis and fibrous
dysplasia

Any bone, especially long bones, such as the
tibia and clavicle

Avulsion fracture

Delayed union

Nonunion

Malunion

Acute chondral and
osteochondral
fractures

Osteochondritis
dissecans

Avulsion injuries

Improper fracture
healing


* From Datir AP, Saini A, Connell A, et al: Stress-related bone injuries with emphasis on MRI. Clin Radiol 62:828, 2007.

From Perumal V, Roberts CS: (ii) Factors contributing to non-union of fractures. Curr Orthop 21:258, 2007.

Fracture that heals in an improper position
Excessive angular or rotational deformity
Adults: leads to deformity that may require surgical correction
Children: often temporary phenomenon that may disappear spontaneously with further skeletal
growth

Fracture site fails to heal completely during a period of 6-9 months after the injury
Characterized by a pseudarthrosis consisting of a synovium-lined cavity and fluid typically
related to persistent motion at the nonunion site
Local causes†: infection, mechanical instability, inadequate vascularity, poor bone contact,
and iatrogenic causes
Systemic causes†: malnutrition, vitamin deficiency, smoking, medications, systemic medical
conditions (diabetes), metabolic bone disorders

Conversion of fibrocartilage to bone is delayed or temporarily stopped

Osseous fragment is pulled from the parent bone by a tendon, ligament, or portion of the joint
capsule

Fragmentation and possible separation of a portion of the articular surface
Adolescent onset most frequent, but occurs from childhood to middle age
Male > female
Symptoms and signs usually begin in patients between ages 15 and 20 years; painful or
painless joint effusion, joint locking, clicking, and limitation of motion
Significant history of trauma in 50% of cases
MR arthrography and computed tomographic arthrography are the most useful imaging

techniques

Not visible on radiographs
Bone marrow edema seen on MR imaging; decreased signal intensity on T1-w images;
increased signal on short tau inversion recovery (STIR)
May be associated with microfractures

Sites of trauma as a result of direct blow,
shear forces, impaction of one bone upon
another, or traction forces from avulsion
injury

Bone contusions
(bone bruises)

CHAPTER 1
Introduction to Skeletal Disorders: General Concepts
7


CHAPTER 1

8

TAB L E 1- 5

Introduction to Skeletal Disorders: General Concepts

Fractures in Children: Concepts and Terminology


Entity

Classification

Typical Sites of Involvement

Characteristics

Incomplete
fractures

Greenstick fracture

Proximal metaphysis of the tibia and
the middle third of the radius and
ulna
Distal end of radius and ulna and,
less commonly, the tibia

Incomplete fracture that perforates one cortex, extends
into the medullary bone, and compresses the opposite
cortex
Incomplete fracture resulting in buckling of the cortex
Usually involves a longitudinal compression force
insufficient to create a complete discontinuity of
the bone
Most frequent in children and osteoporotic persons
Combined compressive and angular forces result in a
combination of greenstick and torus fractures
Most frequent in children

Plastic response of a long tubular bone to longitudinal
stress
Bowing occurs in the absence of cortical discontinuity; in
the case of neighboring bones (radius and ulna or
tibia and fibula), one bone typically fractures or
dislocates, whereas bowing is identified in the
adjacent bone
Seen almost exclusively in children

Torus fracture

Lead pipe fracture

Radius

Bowing fracture

Radius and ulna; less commonly, the
clavicle, ribs, tibia, humerus,
fibula, and femur

Toddler fractures

Distal tibial diaphysis, fibula, femur,
metatarsal bones, and, less
commonly, the calcaneus, cuboid
bone, pubic rami, or patella

Acute onset of fracture in children between the ages of
1 and 3 years

Radiographs may initially be negative; scintigraphy useful
in detecting such occult fractures
Classic toddler fracture: nondisplaced, oblique fracture of
the distal tibial diaphysis

Trauma to
synchondroses
(growth plate
injuries)

Distal end of radius (50%)
Distal end of humerus (17%)
Distal end of tibia (11%)
Distal end of fibula (9%)
Distal end of ulna (6%)
Proximal end of humerus (3%)

Up to 15% of all fractures to the tubular bones in
children younger than 16 years of age involve the
growth plate and neighboring bone
25%-30% of patients develop some degree of growth
deformity

Salter-Harris
classification:
Type I (6%)

Type II (75%)

Type III (8%)

Type IV (10%)
Type V (1%)

Chronic stress injury

Growth centers of the distal end of
the radius and ulna in competitive
gymnasts; also proximal portion of
the humerus, distal ends of the
femur and tibia in other young
athletes

Pure epiphyseal separation; fracture of cartilaginous
growth plate; no fracture of adjacent bones
Slipped capital femoral epiphysis
Growth plate fracture with associated metaphyseal
fracture; metaphyseal fragment termed ThurstonHolland fragment or “corner sign”
Growth plate fracture with associated vertically oriented
epiphyseal fracture
Vertical fracture through the epiphysis, growth plate, and
metaphysis
Crushing or compressive injury of the growth plate with
no associated osseous fracture
Frequently overlooked
Chronic application of stress to the developing growth
center in vigorous or repetitious physical activity
Part of the physis appears widened and irregular with
accompanying sclerosis of the adjacent metaphysis;
often unilateral or asymmetric distribution



CHAPTER 1
TAB L E 1- 5

Introduction to Skeletal Disorders: General Concepts

Fractures in Children: Concepts and Terminology—cont’d

Entity

Classification

Typical Sites of Involvement

Characteristics

Child abuse

Traumatic abuse of
children

Fractures:
• Ribs
• Humerus
• Femur
• Tibia
• Small bones of hands and feet
• Skull
• Spine (rare)
• Sternum (rare)

• Lateral portion of clavicle (rare)
• Scapula (rare)

An estimated 2.8 million children are abused and
2000-5000 deaths are attributed to child abuse in the
United States annually
About 10% of children younger than the age of 5 years
seen for trauma by emergency room physicians have
inflicted injuries that are detectable radiographically
in 50%-70% of cases
Typical age range is between 1 and 4 years; after this
age, children generally are able to escape the abuser
or at least verbalize what has occurred
Humeral fractures in infants and femoral fractures in
crawling children should raise suspicion of abuse

Imaging findings
Fractures in different phases of healing, subperiosteal
hemorrhage with periostitis, metaphyseal corner
fractures, physeal injuries, and transverse diaphyseal
or metaphyseal fractures
Differential diagnosis
Accidental fractures such as torus fractures of the distal
end of radius, toddler’s fractures of the tibia,
clavicular and skull fractures; normal periostitis of
infancy, metaphyseal changes of normal growth,
congenital insensitivity to pain, rickets, osteogenesis
imperfecta, metaphyseal and spondylometaphyseal
dysplasia, Menkes kinky hair syndrome, congenital
syphilis, and infantile cortical hyperostosis (Caffey

disease)

9


10

CHAPTER 1

TAB L E 1- 6

Introduction to Skeletal Disorders: General Concepts

Articular Injuries: Concepts and Terminology

Entity

Typical Sites of Involvement

Characteristics

Joint effusion

Knee
Elbow
Tibiotalar joint
Hip
Glenohumeral joint

Accumulation of excessive synovial fluid within joint

Bland effusion associated with acute injury or internal joint
derangement
Nonbloody effusions usually appear 12-24 hours after injury
Absence of effusion with severe trauma may indicate capsular
rupture of such a degree that fluid extravasates into the soft
tissues surrounding the joint (especially the knee)
Proliferative effusion associated with synovial proliferation as in
inflammatory arthropathy and villonodular synovitis
Pyarthrosis: purulent material in joint from pyogenic septic arthritis

Hemarthrosis

Any injured joint

Accumulation of blood within joint
Hemarthroses usually result in joint effusion within the first few
hours after injury
May result from acute ligament injury, villonodular synovitis,
hemophilia, synovial hemangioma, or other articular diseases

Lipohemarthrosis

Knee
Glenohumeral joint
Hip

Accumulation of blood and lipid material within synovial joint
Fat-blood interface seen on cross-table horizontal beam lateral
radiographs and on transaxial and sagittal MR images
Double fluid-fluid levels on MR images are more specific for

lipohemarthrosis than a single fluid-fluid level
Usually related to acute intraarticular fracture

Pneumolipohemarthrosis

Hip

Accumulation of gas, blood, and lipid material within synovial joint
Typically seen after fracture-dislocation
Most evident on CT scans

Sprain

Acromioclavicular joint
Tibiotalar joint
Knee
Elbow

Grade I: Mild sprain—stretching of the ligament but no tear
Grade II: Moderate sprain—partial ligamentous disruption
Grade III: Complete ligamentous rupture (with or without dislocation)

Subluxation

Glenohumeral joint, patellofemoral
joint, and many other sites

Partial loss of contact between two osseous surfaces that normally
articulate


Dislocation

Glenohumeral joint, acromioclavicular
joint, patellofemoral joint, hip,
apophyseal joints, and many
other sites

Complete loss of contact between two osseous surfaces that normally
articulate

Trauma to symphyses

Symphysis pubis, discovertebral joint,
and manubriosternal joint

Abnormal separation of a joint containing fibrocartilage that normally
is only slightly movable
Cartilaginous nodes, posttraumatic annular vacuum cleft, limbus
vertebrae, and apophyseal ring avulsion fractures resulting from
discovertebral trauma

Heterotopic ossification

Large muscle groups in thigh, leg,
upper arm

Self-limiting posttraumatic myositis ossificans
Usually results from ossification of a chronic muscle hematoma
Imaging findings
Faint calcific intermuscular or intramuscular shadow may appear

within 2-6 weeks of injury
Well-defined region of ossification aligned parallel to the long axis
of the tibia and fibula may be evident within 6-8 weeks
Zonal phenomenon—ossific periphery with radiolucent center
Cleavage plane may be evident between ossification and adjacent
bone, helping to differentiate it from parosteal osteosarcoma
Associated periostitis may relate to subperiosteal hemorrhage
May be surrounded by edema seen on MR images
Differential diagnosis
Aggressive neoplasms such as parosteal, periosteal, and soft tissue
osteosarcoma, and Ewing’s sarcoma, liposarcoma, and synovial
sarcoma


Female : male,
10 : 1

Male = female

Female

>25

>40

Secondary
osteoarthrosis

Erosive
inflammatory

(Erosive)
osteoarthritis

Sex

>40

Typical Age
of Onset
(Years)

Hand

Glenohumeral joint
Elbow
Knee
Hip
Hand
Foot
Sacroiliac joint
Acromioclavicular joint

Knee
Hip
Hand
Foot
Acromioclavicular joint
Sacroiliac joint

Target Sites of

Involvement

Clinical findings
Acute, inflammatory painful episodes of swelling and erythema
overlying the interphalangeal joints of the fingers
Prominent subluxation and osseous nodules (Heberden nodes)
May clinically resemble synovial inflammatory diseases

Unique form of inflammatory interphalangeal osteoarthritis

Articular degeneration that is produced by alterations from a
preexisting affliction; some of these are as follows:
Previous septic arthritis or inflammatory arthritis, slipped
capital epiphysis, developmental dysplasia of the hip,
fracture or dislocation, obesity, Legg-Calvé-Perthes disease,
osteonecrosis, acromegaly, ochronosis, and occupational
or athletic injury
Also occurs with crystal deposition diseases, synovial
inflammatory processes, and other articular diseases
Clinical findings
Same as those of primary osteoarthrosis; findings may coexist
with, or be obscured by, those of the primary disorder

Articular degeneration in the absence of any obvious
underlying abnormality
Accompanies aging
Clinical findings
Variable, depending on site of involvement
Periarticular bony enlargement; e.g., Heberden nodes
Pain and tenderness variable

Joint stiffness and decreased mobility
Joint crepitus
Occasional instability
Subluxation and deformity

Clinical Characteristics

Degenerative Joint Disease and Related Disorders

Primary
osteoarthrosis

Entity

TABLE 1-7

Central erosions
Nonuniform joint-space narrowing
Subchondral sclerosis
Osteophytes
Subluxation

Continued

(See Primary osteoarthrosis)
Appearance of osteoarthrosis may obscure
(or be obscured by) that of the primary
articular process

Nonuniform or, less commonly, uniform joint

space narrowing
Osteophytes
Subchondral sclerosis
Subchondral cysts
Subluxation, deformity, malalignment
Buttressing
Intraarticular osseous bodies; rarely,
secondary synovial osteochondromatosis
Absence of soft tissue swelling
Absence of osteoporosis
Fibrous ankylosis (rare)
Unilateral or bilateral asymmetric distribution

General Imaging Findings

CHAPTER 1
Introduction to Skeletal Disorders: General Concepts
11


Male > female
Thoracic spine
Cervical spine
Lumbar spine
T7-T11 most common
segments

C5-C7
T2-T5
T10-T12

L4-S1
Discovertebral junction
Uncovertebral joint
Apophyseal joint
Costovertebral joint

Target Sites of
Involvement
Clinical Characteristics

DISH affects 25% of men and 15% of women older than
50 years of age
Clinical findings
Symptoms are mild in comparison with the often dramatic
radiographic signs
Middle to lower back pain and stiffness
Restricted motion
Recurrent Achilles tendinosus
Recurrent “tennis elbow”
Cervical dysphagia
Palpable calcaneal, patellar, and olecranon enthesophytes

Degenerative spine disease includes:
Intervertebral osteochondrosis
Spondylosis deformans
Uncovertebral osteoarthrosis
Apophyseal joint osteoarthrosis
Costovertebral joint osteoarthrosis
Clinical findings
Variable, depending on anatomic site and severity

Symptoms range from absent to severe and include acute
or chronic pain, stiffness, radiculopathy (rare), and
associated muscle spasm
Poor correlation between symptoms and radiographic findings;
patients with severe degenerative changes may have
minimal or no symptoms, whereas those with minimal
degenerative changes may have considerable symptoms

Axial skeleton:
Flowing hyperostosis: thick (1-20 mm)
linear shield of ossification along the
anterolateral aspect of the spine (see
Diagnostic criteria below)
Appendicular skeleton:
Enthesopathy and ligament ossification
about the pelvis, hip, knee, foot, heel,
and other extraaxial sites
Diagnostic criteria
1. Flowing calcification and ossification
along the anterolateral aspect of at least
four contiguous vertebral body segments
with or without associated localized
pointed excrescences at the intervening
vertebral body—intervertebral disc
junctions
2. Relative preservation of intervertebral
disc height in the involved vertebral
segment and absence of extensive
degenerative disc disease
3. Absence of apophyseal joint bony

ankylosis and sacroiliac joint erosion,
sclerosis, or intraarticular osseous fusion

Spondylosis deformans:
Osteophytes and osseous ridging
Intervertebral osteochondrosis:
Disc space narrowing
Intradiscal vacuum phenomenon
Disc calcification (rare)
Subchondral bone sclerosis
Schmorl (cartilaginous) nodes
Uncovertebral joint osteoarthrosis:
Sclerosis, hypertrophy, and joint space
narrowing
Apophyseal (facet) joint osteoarthrosis:
Sclerosis, hypertrophy, joint space
narrowing, subluxation, capsular
laxity, and synovial cysts
Frequently contributes to foraminal
stenosis

General Imaging Findings

CHAPTER 1

Diffuse idiopathic
skeletal
hyperostosis
(DISH)


>50

Sex
Male = female

Typical Age
of Onset
(Years)

Degenerative Joint Disease and Related Disorders—cont’d

Degenerative spine >30
disease

Entity

TABLE 1-7

12

Introduction to Skeletal Disorders: General Concepts


25-55

5-10

Juvenile
idiopathic
arthritis†


Typical Age
of Onset
(Years)

Variable,
depending
on
disorder

Female : male,
2 or 3 : 1

Sex

Hand
Wrist
Knee
Cervical spine
Foot
Ankle
Elbow
Heel
Hip

Hand
Foot
Wrist
Knee
Elbow

Glenohumeral joint
Acromioclavicular joint
Cervical spine

Target Sites of
Involvement

Inflammatory Articular Disorders

Rheumatoid
arthritis

Entity

TABLE 1-8

Soft tissue swelling
Periarticular osteoporosis with metaphyseal lucent
bands
Diffuse joint space loss (late finding)
Erosions (late finding)
Periostitis
Growth disturbances
Apophyseal joint ankylosis
Extraaxial joint ankylosis
Atlantoaxial instability
Bony proliferation and periostitis
Epiphyseal compression fractures

Several arthropathies have been identified in children

Disorders
1. Systemic arthritis
2. Oligoarthritis
Persistent
Extended
3. Polyarthritis
Rheumatoid factor negative
Rheumatoid factor positive
4. Enthesitis-related arthritis
5. Psoriatic arthritis
6. Other
Clinical findings
Variable, depending on disorder
Subcutaneous nodules
Acute joint swelling, pain, and erythema
Systemic manifestations:
Vasculitis
Hepatosplenomegaly
Iridocyclitis

Introduction to Skeletal Disorders: General Concepts
Continued

Laboratory and Imaging Findings

Laboratory findings:
Normochromic or hypochromic normocytic anemia
(common)
Leukocytes: normal, elevated, or, infrequently,
decreased

Erythrocyte sedimentation rate: markedly elevated
Rheumatoid factor: present in high titers
Positive LE phenomenon (8%-27% of patients)
Imaging findings
Fusiform soft tissue swelling (early finding)
Concentric joint space narrowing (early finding)
Marginal and central subchondral erosions
Subchondral cysts
Cortical atrophy and osteolysis
Absent or mild sclerosis
Periarticular osteoporosis
Synovial cysts
Joint instability, particularly atlantoaxial joint
Fibrous ankylosis, and infrequently, bony ankylosis
Deformity, subluxation, dislocation
Pathologic fractures

Clinical Characteristics
Bilateral symmetric polyarticular synovial
inflammatory process
Five to 15 times as common as ankylosing spondylitis
Clinical findings
Acute or chronic episodes of painful joint swelling
Prodromal symptoms: fatigue, anorexia, weight loss,
malaise, muscular pain, and stiffness
Capsular and ligamentous laxity
Muscular contraction and spasm
Bursitis, tendinitis, and tenosynovitis
Diagnostic criteria*
1. Morning stiffness in and around joints lasting at

least 1 hour before maximal improvement
2. Soft tissue swelling (arthritis) of three or more
joint areas observed by a physician
3. Swelling (arthritis) of the proximal interphalangeal,
metacarpophalangeal, or wrist joints
4. Symmetric swelling (arthritis)
5. Rheumatoid nodules
6. The presence of rheumatoid factor
7. Radiographic erosions or periarticular osteopenia,
or both, in hand or wrist joints, or in both
Rheumatoid arthritis is defined by the presence of
four or more criteria; criteria 1 through 4 must
have been present for at least 6 weeks

CHAPTER 1
13


15-35

20-50

Psoriatic
arthropathy

Typical Age
of Onset
(Years)
Sacroiliac joint
Thoracolumbar spine

Cervical spine
Symphysis pubis
Hip
Shoulder
Heel

Hand
Foot
Sacroiliac joint
Thoracolumbar spine
Cervical spine

Male =
female

Target Sites of
Involvement

Male : female,
4 : 1 to
10 : 1

Sex

Inflammatory Articular Disorders—cont’d

Ankylosing
spondylitis

Entity


TABLE 1-8

Laboratory findings
HLA-B27 antigen present in as many as 60% of
patients with psoriatic arthropathy
Mild anemia
Elevated erythrocyte sedimentation rate
Elevated serum uric acid levels (occasionally)
Negative for rheumatoid factor
Imaging findings
Axial skeleton:
Paravertebral ossification (nonmarginal
parasyndesmophytes)
Unilateral or bilateral asymmetric sacroiliitis
Atlantoaxial instability
Extraaxial skeleton:
Soft tissue swelling: periarticular or involving
entire digit (sausage digit)
Absence of osteoporosis
Severe joint space destruction with marginal
erosions

CHAPTER 1

Seronegative spondyloarthropathy
Less common than ankylosing spondylitis
Two to 6% of patients with psoriatic skin lesions
have associated psoriatic arthropathy
Clinical patterns

1. Polyarthritis with distal and proximal
interphalangeal joint involvement
2. Deforming arthritis characterized by ankylosis
and arthritis mutilans
3. Symmetric rheumatoid-like arthritis (rare)
4. Asymmetric oligoarthritis or monoarthritis
5. Combination of spondyloarthropathy and
sacroiliitis
Signs and symptoms
Long history of psoriatic skin lesions: patchy, scaly
macular lesions
Nail changes: pitting, discoloration, splintering,
erosion, thickening, and detachment

Laboratory and Imaging Findings

Laboratory findings:
Elevated erythrocyte sedimentation rate
Negative rheumatoid and LE factors
HLA-B27 histocompatibility antigen present in 90% of
patients (6 to 8% of general population)
Radiographic findings
Spine: marginal syndesmophytes, erosions, ligament
ossification (see Tables 3-9 and 3-10)
Sacroiliac joints: bilateral symmetric involvement; joint
erosion initially with eventual ankylosis
Extraaxial skeleton: joint erosions; partial or complete
osseous ankylosis; enthesopathy

Clinical Characteristics

Most common seronegative spondyloarthropathy
Clinical findings
Axial skeleton:
Middle and low back pain and stiffness
Limited lumbar and thoracic spine motion
Limited chest expansion (1 inch or less)
Sacroiliac joint pain
Radiating pain to lower extremity (50%)
Muscle spasm
Increased thoracic kyphosis
Extraaxial skeleton:
As many as 50% of patients affected
Mild symmetric involvement is typical
Pain, tenderness, and swelling
Extraskeletal findings:
Iritis (20% of cases)
Aortic insufficiency and aneurysms
Pulmonary fibrosis (upper lobes)
Pleuritis
Inflammatory bowel disease
Amyloidosis (especially kidney)

14

Introduction to Skeletal Disorders: General Concepts


×