Ebook Bone and joint disorders differential diagnosis in conventional radiology (2nd edition): Part 1

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Bone and Joint Disorders
Differential Diagnosis in Conventional Radiology

Francis A. Burgener, M.D.

Martti Kormano, M.D.

Tomi Pudas, M.D.

Professor of Radiology
University of Rochester
Medical Center
Rochester, N.Y., U.S.A.

Formerly Professor and Chairman
Department of Radiology

University of Turku
Turku, Finland

Department of Radiology
University of Turku
Turku, Finland

2nd revised edition
1108 illustrations

Thieme
Stuttgart · New York

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IV
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V

Preface

Conventional radiography remains the backbone of
musculoskeletal radiology despite the advent of newer and
more exciting imaging techniques such as computed tomography, magnetic resonance imaging, and, most recently,
positron emission tomography. In contrast to many of these
newer methods, conventional radiography is practiced not
only by radiologists but also by a large number of clinicians
and surgeons. With each examination, one is confronted
with radiologic findings that require interpretation in order
to arrive at a general diagnostic impression and a reasonable
differential diagnosis. To assist the film reader in attaining
this goal, this book is based upon radiographic findings unlike most other textbooks in radiology that are disease
oriented. Since many diseases present radiographically in a
variety of manifestations, some overlap in the text is unavoidable. To minimize repetition the differential diagnosis
of a radiographic finding is presented in tabular form
whenever feasible. Most tables do not only list the various

diseases that my present radiologically in a a specific pattern, but also describe in succinct form other characteristically associated radiographic findings and pertinent clinical
data. Radiographic illustrations and drawings are included to
demonstrate visually the radiographic features under discussion.
The transition from film to digital radiography had the
greatest impact on conventional radiology since the publication of the last edition. This change, however, did not affect
the way radiologic diagnoses are ascertained. Since the publication of the last edition the name of a few disorders has
changed (e. g., histiocytosis X to Langerhans cell histiocytosis) and a few disease are newly recognized (e. g.,
femoroacetabular impingement). These facts were taken
into account in the new edition. The chapters “Localized
Bone Lesions“ and “Joint Diseases“ were completely rewritten and newly illustrated, since I took them over from Dr.
Kormano. The chapter “Trauma and Fractures“ also under

went a major overhaul by the inclusion of specific fracture
sites. In the remaining chapters of the book the text was updated, many illustrations replaced, and large numbers of
new illustrations added.
A changing of the guard has also taken place. Since Dr.
Martti Kormano‘s professional endeavors do no longer include clinical radiology, he felt no longer up the task to update his original contributions to the text. He was however
very fortunate to find in Dr. Tomi Pudas a very talented
young radiologist to take over the revision of the chapters
originally prepared by him.
I hope this new edition will be as well received as its predecessors in the past that were translated into five foreign
languages. The concept of an imaging pattern approach in
tabular form rather than a disease oriented text was introduced in 1985 with our original edition Differential Diagnosis
in Conventional Radiology and has since been adopted by
many authors. I feel complimented by the old cliché, “imitation is the sincerest form of flattery.“
This book is meant for physicians with some experience in
musculoskeletal radiology who wish to strengthen their diagnostic acumen. It is a comprehensive outline of radiographic findings and it should be particularity useful to radiology residents preparing for their specialist examination,
especially since the exposure to conventional radiography
during their training continuously decreased in the past in
favor of newer imaging modalities. Any physician involved in

the interpretation of conventional bone radiographic examinations should find this book helpful in direct proportion to
his or her curiosity.
It is my hope that this new edition will be as well received
as the previous ones by medical students, residents, radiologists, and physicians involved in the interpretation of conventional bone radiographs.

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Francis A. Burgener, M. D.


VI

Acknowledgements

It is impossible to thank individually all those who helped to
prepare the third edition of this textbook. I wish to acknowledge the staff of our publisher Thieme, in particular Dr. Clifford Bergman and Mr. Gert A. Krüger.
I am deeply indebted to Dr. Gertrud Gollman, Steinach am
Attersee, Austria, who translated the last edition of this text
into German and suggested many alterations and corrections, which have been incorporated into this new edition.
My gratitude goes to all the radiologists whose cooperation made available illustrative cases to compliment the
original collection or to replace older illustrations. I am indebted to Drs. Steven P. Meyers, Johnny U. V. Monu, and Gwy
Suk Seo, all staff members of the University of Rochester
Radiology Department, and to the former residents Drs. John
M. Fitzgerald and Wael E. A. Saad for providing selected
cases.

I wish to express also many thanks to Jeanette Griebel,
Iona Mackey, and Marcella Maier for their assistance in preparing the references and to Shirley Cappiello for her general
assistance. Last, but not least, I am most grateful to Alyce
Norder who left the University and me after 30 years for the

richness of the industry. She is the only person capable of
deciphering my longhand and, as in the past, did a superb
job in typing, editing, and proofreading the manuscript of
the new edition of this text. Despite her heavy workload as
executive assistant in her new endeavor. Alyce was kind
enough to perform this task in her spare time, for which I am
greatly appreciative.
Finally I appreciate the support of my wife Therese, who
has generously given her precious family time for the preparation of this book.
Francis A. Burgener, M.D.

I would like to express my deepest gratitude to honorary
professor Martti Kormano who invited me to carry on his
work in this new edition. I continue to admire the massive
work that he and Dr. Burgener originally put into the project
in the early nineteen-eighties. The hundreds of hours which
Dr. Kormano and I have spent together editing this edition
have been a great pleasure. It was a fascinating time in my
life.
I especially want to thank Drs. Kimmo Mattila and Seppo
Koskinen for introducing me to musculoskeletal radiology,
and for their extraordinary teaching and support. Many
thanks also belong to Drs. Erkki Svedström, Risto Elo, and
Peter B. Dean for encouraging me on my way in the field of

radiology. The many fascinating discussions I have had with
Drs. Seppo Kortelainen and Teemu Paavilainen brought me
much delight, on non-radiological topics as much as on professional subjects.
I also express sincere thanks to the staff of the publishers,
Thieme, especially to Dr. Clifford Bergman and Mr. Gert

Krüger. Finally, much gratitude is due to Mr. Markku
Livanaien for his valuable assistance with technical questions, and to Ms. Pirjo Helanko for all her help with general
matters. Many other individuals helped in various ways with
this project, and though I cannot name them all, I am grateful
for their contributions.
Tomi Pudas, M.D.

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VII

Contents

1 Osteopenia . . . . . . . . . . . . . . . . . . . . . . . . . . .

3

10 Nasal Fossa and Paranasal Sinuses . . . . . . . . 237

Francis A. Burgener

Francis A. Burgener

2 Osteosclerosis . . . . . . . . . . . . . . . . . . . . . . . .

15

11

Francis A. Burgener

Jaws and Teeth . . . . . . . . . . . . . . . . . . . . . . . 245
Francis A. Burgener

3 Periosteal Reactions . . . . . . . . . . . . . . . . . . .

41

12

Francis A. Burgener

Spine and Pelvis . . . . . . . . . . . . . . . . . . . . . . . 255
Martti Kormano and Tomi Pudas

4 Trauma and Fractures . . . . . . . . . . . . . . . . . .

53

13

Francis A. Burgener

Clavicles, Ribs, and Sternum . . . . . . . . . . . . . 305
Martti Kormano and Tomi Pudas

5 Localized Bone Lesions . . . . . . . . . . . . . . . . .

75

Francis A. Burgener

14

Extremities . . . . . . . . . . . . . . . . . . . . . . . . . . . 313
Francis A. Burgener, Martti Kormano,
and Tomi Pudas

6 Joint Diseases . . . . . . . . . . . . . . . . . . . . . . . . . 129
15 Hands and Feet . . . . . . . . . . . . . . . . . . . . . . . 353

Francis A. Burgener

Martti Kormano and Tomi Pudas

7 Joint and Soft-Tissue Calcification . . . . . . . . 189
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 392

Martti Kormano and Tomi Pudas

8 Skull . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 393

Francis A. Burgener

9 Orbits . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
Francis A. Burgener

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VIII

Abbreviations

ABC
AC
ACTH
AIDS
ALL
AML
ANCA
ANT
AP
AV
AVF
AVM
AVN
Bx
Ca
CLL
CNS
CPP
CPPD

aneurysmal bone cyst
acromioclavicular (joint)
adrenocorticotropic hormone

acquired immune deficiencly syndrome
acute lymphoblastic leukemia
acute myeloblastic leukemia
antineutrophil cytoplasmotic autoantibodies
anterior
anteroposterior
arteriovenous
arteriovenous fistula
arteriovenous malformation
avascular necrosis
biopsy
calcium
chronic lymphatic leukemia
central nervous system
calcium pyrophosphate dihydrate crystals
calcium pyrophosphate dihydrate deposition
disease
CRMO chronic recurrent multifocal osteomyelitis
CT
computed tomography
D
disease
DD
differential diagnosis
DDH
development dysplasia of the hip
DIP
distal interphalangeal (joint)
DISH diffuse idiopathic skeletal hyperostosis
DISI

dorsal intercalated segmental instability
EAC
external auditory canal
EG
eosinophilic granuloma
F
female
HAD
calcium hydroxyapatite crystals
HADD calcium hydroxyapatite crystal deposition disease
Hb
hemoglobin
HD
Hodgkin disease
HIV
human immunodeficiency virus
Hx
history
IAC
internal auditory canal
IM
intramuscular

IP
IV
L
LCH
LE
M
MAI

MCP
MFH
MPS
MR
MRI
MS
MTP
NHL
NUC
PA
PATH
PET
PIP
PNET
PVNS
RA
RBC
RES
RSD
SC
SI
SLAC
SLE
STT
TB
TFC
TFCC
TMJ
TNM
VISI

WBC

interphalangeal (joint)
intravenous
left
Langerhans cell histiocytosis
lupus erythematosus
male
Mycobacterium avium intracellulare
metacarpophalangeal (joint)
malignant fibrous histiocytoma
mucopolysaccharidosis
magnetic resonance
magnetic resonance imaging
multiple sclerosis
metatarsophalangeal (joint)
non-Hodgkin lymphoma
nuclear medicine
posteroanterior
pathology
positron emission tomography
proximal interphalangeal (joint)
primitive neuroectodermal tumor
pigmented villonodular synovitis
rheumatoid arthritis
red blood cell
reticuloendothelial system
reflex sympathetic dystrophy
sternoclavicular (joint)
sacroiliac (joint)

scapholunate advanced collapse
systemic lupus erythematosus
scaphotrapeziotrapezoidal
tuberculosis
triangular fibrocartilage
triangular fibrocartilage complex
temporomandibular joint
tumor-node-metastasis
volar intercalated segmental instability
white blood cells

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Bone

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Osteopenia

Osteopenia is defined as a decrease in bone density caused
by reduced bone formation and/or increased bone resorption. Reduction in bone formation may result from either inadequate matrix formation (e.g., disuse osteoporosis and
protein deficiency of any etiology) or inadequate matrix calcification (e. g., osteomalacia). Primary hyperparathyroidism
is an example of too much resorption of both bone matrix
and mineral. A combination of these causes results in the undermineralization present in the majority of osteopenic disorders. Furthermore replacement of bone matrix by benign
or malignant bone proliferation (e.g. thalassemia, multiple
myeloma and leukemia) or bone marrow disease (e.g.
metastases, infections and storage diseases) may also result
in osteopenia.
Approximately 30 % of the bone mineral must be lost
before a difference in the bone density can be detected by
conventional radiography. More sensitive techniques useful
for earlier detection and quantification of osteopenia include
axial computed tomography and photon or x-ray absorptiometry. It should also be borne in mind that the normal
bone density changes with age, increasing from infancy to
age 35−40 and then progressively decreasing at the rate of
8 % per decade in women and 3 % in men.
The radiographic findings of osteopenia are loss of bone
density and cortical thinning. Osteopenia may either be
generalized or localized, and its differential diagnosis is discussed separately in Tables 1.1 and 1.2.
In osteoporosis, a combination of loss of bone density and
cortical thinning may result in an apparent increase in density of the cortex and vertebral endplates, that appear as

a

thin, sharp lines (Figs. 1.1 and 1.2). Bone resorption occurs
preferentially in the transverse trabeculae, while the
trabeculae along stress lines are accentuated. Resorption of

all trabeculae in a vertebral body produces the “empty box”
sign. As a result of compression fractures the vertebral body
may depict a depressed endplate or become wedge-shaped,
biconcave (fish vertebra) or uniformly compressed (pancake
vertebral body). Cartilaginous (Schmorl’s) nodes are caused
by displacement of a portion of the intervertebral disc into
the vertebral body. With the exception of osteogenesis imperfecta, bones do not bend in osteoporosis. A predisposition
towards fractures, however, exists in the brittle bones, especially in the vertebral bodies, ribs, hips and wrists. Fracture
healing is delayed and the callus formation poor. Abundant
callus formation in osteopenic bones may occur, however,
with exogenous (iatrogenic) or endogenous (Cushing’s syndrome) hypercortisolism and osteogenesis imperfecta. In
osteoporosis, serum calcium, phosphorus and alkaline
phosphatase are normal.
In osteomalacia, a nonspecific loss of bone density is often
the only radiographic sign. Blurring of both cortical margins
and trabeculae results in a “ground glass” appearance of the
involved bone and is more characteristic. This is often most
obvious in the vertebral bodies. In the skull, a blurred mottled
appearance similar to hyperparathyroidism is characteristic.
Bones are softened and have a tendency to bend resulting in
deformities commonly found in the thorax, vertebral
column, pelvis and extremities. Pseudofractures (Looser’s
zones or Milkman’s syndrome) occur frequently and represent infractions with incomplete healing. They are found in

b

Fig. 1.1 Osteopenia. a Osteoporosis: Deossified, biconcave vertebral bodies (fish vertebrae) with thin but dense-appearing endplates and prominent vertical trabeculae. The superior endplates
typically are affected more severely. b Osteomalacia: Uniform
deossification with loss of trabecular detail (“ground-glass appearance”) and compression fractures. Fish vertebrae tend to be

c
smoother than in osteoporosis and involve superior and inferior
endplates with equal severity. c Hyperparathyroidism: A “rugger
jersey spine” is usually only found in secondary hyperparathyroidism (renal osteodystrophy), whereas primary hyperparathyroidism
depicts a bony texture similar to osteomalacia.

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Bone

a
b
Fig. 1.2 Osteoporosis (a), osteomalacia (b) and hyperparathyroidism (c and d). Osteoporosis (a): Thin sharply defined endplates with accentuation of the vertical trabeculae are seen.
Osteomalacia (b): Uniformly biconcave vertebral bodies with
poorly defined endplates and blurred trabeculae are seen. Primary

c
d
hyperparathyroidism (c): Thin poorly defined endplates with blurring of the trabecular pattern in the vertebral bodies are seen. Secondary hyperparathyroidism (d): Blurring of the trabecular pattern
in the vertebral bodies is associated with thickening and sclerosis
of the superior and inferior endplates (“rugger jersey spine”).

the scapula (lateral margin), ribs, clavicle, ischial and pubic
rami, femur (especially medial aspect of the neck), and other
long bones. Characteristic laboratory findings in osteomalacia include a slightly low to normal serum calcium, a low
serum phosphorus and an elevated alkaline phosphatase.
Bony lesions are found in less than half of the patients

with hyperparathyroidism. Subperiosteal resorption along

the radial margin of the phalanges is virtually pathognomonic. These erosions occur most often in the proximal and
middle phalanges of the index and middle finger (Fig. 1.3).
Absorption of the terminal tufts and cortical striations (“tunneling of the cortex”) are commonly associated with this
condition. Endosteal resorption occurs in long bones. Resorption may also be evident in the acromial ends of the

Fig. 1.3 Hyperparathyroidism of the hand. Subperiosteal resorption and cortical striations, usually best seen on the radial margins of proximal and middle phalanges of second and third finger.
A magnified view of these findings is demonstrated in insert a,
whereas insert b shows a normal cortex for comparison. Additional
findings include resorption of the tufts, periarticular soft-tissue
calcifications, brown tumors (third metacarpal and capitatum),
and joint cartilage calcification (often in the triangular fibrocartilage between ulna and corresponding part of the proximal carpal
row).

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1 Osteopenia
clavicles, the sacroiliac joints, the symphysis, in the calcaneus at the insertion of the plantar fascia and in the ribs
(usually in their upper borders). The bone is softened resulting in secondary deformities such as basilar impression in
the skull and kyphoscoliosis. Cyst-like lesions and so-called
brown tumors occur in tubular and flat bones. While brown
tumors heal after removal of the parathyroid adenoma and
may eventually even become sclerotic, cysts remain unchanged after treatment. Granular deossification of the skull
results in a “salt and pepper” appearance. Resorption of the
lamina dura around the teeth is commonly present. Soft
tissue calcifications (especially arterial and para-articular),
joint cartilage calcifications (especially menisci and the triangular fibrocartilage in the wrist), nephrocalcinosis, and
nephroureterolithiasis are common features of hyper-

5

parathyroidism. Pancreatitis, peptic ulcer disease and gallstones may also be associated. Classic laboratory findings in
primary hyperparathyroidism include a high serum calcium,
a low serum phosphorus, and an elevated alkaline
phosphatase in the presence of bone disease.
An increased bone density is often associated with secondary hyperparathyroidism (renal osteodystrophy). In
these cases thickening of the superior and inferior endplates
of the vertebral bodies can result in a “rugger jersey spine”.
The skeletal changes in different forms of hyperparathyroidism are identical, although brown tumors are more common in primary hyperparathyroidism, whereas osteosclerosis and extensive soft-tissue calcifications are more often
found in secondary hyperparathyroidism.

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Bone

Table 1.1 Differential Diagnosis of Generalized Osteopenia
Etiology

Comments

Osteoporosis

Laboratory findings: serum calcium, phosphorus and alkaline phosphatase all normal.

Senile or postmenopausal

Most common form of osteoporosis. Females affected more often and more severely than
males. Compression fractures typically spare the less weight-bearing cervical and upper
thoracic spine.

Disuse atrophy

Prolonged immobilization from any cause (e.g., neuromuscular disorders, cast).

Protein deficiency (e.g., malnutrition, nephrosis) (Fig. 1.4)

Pure dietary protein deficiency is rare. In underdeveloped countries, extensive osteopenia
is associated with kwashiorkor, a marasmic protein-calorie malnutrition affecting mostly
children. Protein deficiency secondary to malabsorption is more common (see under
osteomalacia). Abnormal protein metabolism is the underlying cause of osteoporosis in
scurvy (vitamin C deficiency) and different endocrinologic disorders.

Juvenile (idiopathic)

Between ages 8 and 14, characterized by abrupt onset of bone pain. Rare, self-limiting disorder with commonly spontaneous healing.

Osteogenesis imperfecta (Fig. 1.5)

Osteogenesis imperfecta congenita (fractures present at birth) and tarda (fractures absent
at birth). Deformities resulting from recurrent fractures in later life and bone bending
characteristic. Both disorders inherited.

Homocystinuria

Inherited disorder that presents radiographically as combination of osteoporosis, Marfanlike changes (e.g., arachnodactyly), and metaphyseal and epiphyseal widening.

Anemia (Fig. 1.6)

Bone marrow hyperplasia causes widening of the medullary space, cortical thinning, and
trabecular resorption by pressure atrophy. Occurs in severe iron deficiency and sickle cell
anemia, but is more pronounced in thalassemia, where a generalized cystic appearance,
particularly of the flat bones, is characteristic.

Bone marrow infiltration (e.g. multiple myeloma, carcinomatosis)
(Fig. 1.7)

Deossification is caused by diffuse infiltration and proliferation of tumor cells in the bone
marrow resulting in endosteal erosions, cortical thinning and trabecular resorption by both
pressure atrophy and destruction. While osteopenia might be the only radiologic manifestation in multiple myeloma and diffuse skeletal bony metastases, patchy osteolytic areas
are often present in these conditions. Bone marrow infiltration associated with cortical
thinning and trabecular resorption can also be found in reticuloses (e.g. Gaucher’s and
Nieman-Pick disease), histiocytoses and hyperlipoproteinemias. In children, leukemia
frequently causes osteopenia.

Connective tissue disease (especially rheumatoid arthritis)

Other more characteristic radiographic findings are often associated with the disease suggesting the correct diagnosis (see Chapter 6).

(continues on page 8)
Fig. 1.4 a, b Scurvy. Characteristic findings include: (1) Osteopenia with markedly thinned cortex, (2) thin, dense, ring-like calcification around the epiphysis (Wimberger’s line), (3) dense, linear
calcifications in the distal metaphysis (“white line of Frankel”), (4) a
small bone spur immediately adjoining the “white line of Frankel”
(Pelkan’s spur), (5) a radiolucent band proximal to the “white line
of Frankel” (Trummerfeld zone), and (6) subperiosteal hemorrhage
(calcifies only after therapy is instituted). Epiphyseal separation

and/or fragmentation in the region of the metaphysis may also be
associated.

a

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1 Osteopenia

7

a

a
b
Fig. 1.5 a, b Osteogenesis imperfecta. Diffuse osteopenia with
bowing deformities of the narrowed (overconstricted) tibia and
fibula shafts with flaring of the metaphyses is seen in anteroposterior (a) and lateral (b) projections.

b
Fig. 1.6 Thalassemia major. Chest (a) and pelvis (b). Generalized, cystic-appearing osteopenia caused by red bone marrow hyperplasia, with main involvement of the central or flat bones
characteristic. Note also the bulbous widening of the anterior ends
of the ribs.

୵ Fig. 1.7 Multiple myeloma presenting as generalized osteopenia
in the spine. In this case, however, extensive destruction of L1 and
the destroyed left pedicle of L5 suggest the malignant process.

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Bone

Table 1.1 (Cont.) Differential Diagnosis of Generalized Osteopenia
Etiology

Comments

Endocrine disorders

Hypogonadism: osteoporosis associated with delayed epiphyseal fusion (e.g., Turner’s syndrome, eunuchoidism). Cushing’s syndrome: chronic excess of glucocorticoids. Addison’s disease: insufficiency of the adrenal cortex. Diabetes mellitus: osteopenia present in about
50 % of patients.
Hyperthyroidism: often associated with cortical striations best seen in metacarpal bones.
See also under hyperparathyroidism in this table.

Drug-induced (e.g., steroids,
heparin) (Fig. 1.8)

Steroids: large dosages over several months. Heparin: 15,000 to 30,000 units for six
months or longer.

Osteomalacia (Fig. 1.9)

Laboratory findings in osteomalacia: serum calcium slightly low to normal; serum phosphorus low; alkaline phosphatase elevated.

Deficient absorption of calcium
and/or phosphorus;

1. vitamin D deficiency

Dietary causes, or lack of sunshine
Adult: osteomalacia. Loss of bone density with blurring of both cortical margins and
trabeculae characteristic. Bowing deformities and pseudofractures occur frequently.
Children: rickets (Fig. 1.10). Most commonly found in premature infants. Develops most
commonly between 6 and 12 months of age. Radiographic features include: indistinct,
frayed and concave metaphyses (“cupping”) with perpendicular trabeculae extending
towards the epiphyseal areas. Delayed appearance of epiphyseal ossification centers with
blurred margins (DD: Scurvy: sharply outlined epiphyses). Bulky growth plates in long
bones result in swelling around the joints and a “rachitic rosary” at the costochondral junctions of the middle ribs.

2. Malabsorption

Diseases of the gastrointestinal tract, hepatobiliary system and pancreas associated with
malabsorption are the most common cause of Vitamin D deficiency in developed countries. Rickets and osteomalacia is commonly associated with sprue, celiac disease, Crohn’s
disease, scleroderma, small bowel fistulas, blind loop syndromes, small intestinal bypass
surgery, and gastric or small bowel resection.

3. Dietary calcium deficiency

Extremely rare.

Defects in renal tubular or intestinal calcium phosphate transport
system:
1. Vitamin D-resistant rickets
(x-linked hypophosphatemia) and
pseudo-vitamin D deficiency rickets
(Figs. 1.11 and 1.12)

Proximal tubular resorption of phosphorus decreased. Inherited (X-linked dominant and autosomal recessive) disorders with similar clinical features (short stature, multiple fractures,
varus or valgus deformities of the knees, bowing deformities of the long bones in the
lower extremities and muscular weakness), but only the latter condition is commonly associated with convulsions. Enthesopathy in the spine may resemble ankylosing spondylitis
but without erosions in the sacroiliac joints.

(continues on page 10)
Fig. 1.8 Steroid-induced osteoporosis. Osteoporosis with thickening and sclerosis of
the compressed end-plates is characteristic of exogenous or endogenous hypercortisolism.

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1 Osteopenia

9

Fig. 1.9 Osteomalacia.
Marked demineralization with
blurring of the inner cortical
margins and loss of trabeculations are characteristic. Several
pseudofractures are seen, presenting as sclerotic transverse
lines in the tibia.

Fig. 1.10 Rickets. Characteristic changes include:
(1) osteopenia, (2) poorly
calcified and defined
epiphyses, (3) widening of
the epiphyseal cartilage
plate, (4) widening, cupping, and fraying of the
metaphyses, (5) periosteal

reactions, and (6) bowing
deformities. Greenstick
fractures are also commonly associated, but not
present in this case.

Fig. 1.11 Vitamin D-resistent
rickets (x-linked hypophosphatemia). Osteopenia
with multiple fractures/pseudofractures and anterior bowing
deformity of the tibia is seen.

Fig. 1.12 Vitamin
D-resistent rickets
(x-lilnked hypophosphatemia). Mild
osteopnia with
bowing deformity
and pseudofracture
in the distal femur
and genu varum is
seen.

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Table 1.1 (Cont.) Differential Diagnosis of Generalized Osteopenia
Etiology

Comments

2. Renal tubular acidosis (Fig. 1.13)

Metabolic acidosis attributed to renal loss of alkali. Pathogenesis of osteomalacia in this
condition is unclear. Commonly associated with nephrocalcinosis and nephrourolithiasis.

3. Fanconi’s syndrome (De ToniDebré-Fanconi syndrome)

Idiopathic or acquired disorder characterized by hypophosphatemia, glucosuria and aminoaciduria. The idiopathic form is often associated with cystinosis (widespread tissue deposition of cystine crystals). The acquired form may be secondary to Wilson’s disease (rare familial disorder with impaired hepatic excretion of copper and characteristic pigmentation
of the cornea [Kayser-Fleischer ring], multiple myeloma and lead or cadmium poisoning.

Chronic anticonvulsant drug
therapy

Anticonvulsants (e.g. Phenytoin) and many tranquilizers induce hepatic enzymes that accelerate degradation of biologically active vitamin D metabolites.

Fibrogenesis imperfecta ossium
and axial osteomalacia

Fibrogenesis imperfecta ossium (axial and appendicular bone involved) and axial
osteomalacia (only axial skeleton involved) are rare disorders found in middle-aged males.
Loss of bone density with a few coarse trabeculae may produce a “fishnet appearance.”
Occasionally, the bone density may increase.

Hypophosphatasia (Fig. 1.14)

Autosomal recessive disorder with a wide spectrum of clinical severity. Generalized deficient bony mineralization is found radiographically. The most severe skeletal involvement is
observed in neonates, in whom the disease is often fatal. In childhood the disorder resembles rickets, but associated irregular lucent extensions into the metaphyses representing uncalcified bone matrix are characteristic. The adult form is characterized by radiolucent bones, pseudofractures, and fractures occurring after minor trauma that show
delayed healing with minimal callus formation. Biochemical hallmark; low alkaline

phosphatase.

Hyperparathyroidism (Figs. 1.15
and 1.16)

Laboratory findings of primary hyperparathyroidism: serum calcium high; serum phosphorus low; alkaline phosphatase elevated in the presence of bone disease.

Primary hyperparathyroidism

Found with parathyroid adenoma, primary chief cell or clear cell hyperplasia of all parathyroid glands, and parathyroid carcinoma.

Secondary hyperparathyroidism

Compensatory mechanism in any state of true hypocalcemia. Usually due to chronic renal
failure, but may also be caused by hypovitaminosis D and malabsorption of calcium. In
chronic renal disease, the skeletal changes are usually a combination of hyperparathyroidism, osteomalacia and osteosclerosis. This complex is best referred to as “renal osteodystrophy .”

Tertiary hyperparathyroidism

Development of an autonomous parathyroid adenoma in chronically overstimulated hyperplastic parathyroid glands (e.g., following renal transplantation).

Fig. 1.13 Renal tubular acidosis. Increased bone density secondary to renal osteodystrophy is seen. Note also the extensive bilateral nephrocalcinosis.

Fig. 1.14 Hypophosphatasia. Osteopenia and a radiolucent lesion (arrows) extending from the growth plate into the distal
femur metaphysis representing uncalcified bone matrix are seen.

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1 Osteopenia

11

Fig. 1.15 Hyperparathyroidism. Subperiosteal resorption best seen along the radial
margin of the proximal phalanges of both
index fingers. Brown tumors involving the
distal phalanx of the left index finger and
the entire right third metacarpal bone. Resorption of the tufts, especially in the
thumbs. The cortex in the metacarpals and
phalanges depicts fine striations.

Fig. 1.16 Hyperparathyroidism. Subperiosteal resorptions seen along the radial
margins of the proximal and middle
phalanges of the second finger and the
middle phalanx of the third finger are virtually diagnostic. Cortical striations are also
evident.

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Table 1.2 Differential Diagnosis of Localized Osteopenia
Etiology

Comments

Disuse atrophy (local immobilization):

1. fracture (more pronounced distal to the fracture site)
2. cast
3. neural paralysis
4. muscular paralysis

Besides identical radiographic features as in generalized osteopenia, the localized form
may also have a patchy appearance due to spotty cortical thinning (e. g., reflex sympathetic dystrophy).

Reflex sympathetic dystrophy (RSD,
Sudeck’s atrophy) (Fig. 1.17)

Rapid development of often patchy osteoporosis associated with painful soft-tissue swelling following trivial trauma. Cerebrovascular disorders, cervical spondylosis, discal herniation, postinfectious states, calcific tendinitis, vasculitis, and neoplasm are other implicated
conditions. Probably of neurovascular origin.

Regional transitory osteoporosis

A painful self-limited osteoporosis in middle-aged or elderly patients. Most often found in
the hip (“transitory demineralization of the femoral head”) , but may also involve any other
major joint. Associated with disability lasting 2 to 4 months.

Shoulder-hand syndrome (Fig. 1.18)

Pain and stiffness in the shoulder combined with pain, swelling and vasomotor phenomena
in the hand following an acute illness (e.g. myocardial infarction, in which condition it is
usually located on the left side). Radiographically, it resembles reflex sympathetic dystrophy.

Burns and frostbites

Radiographic findings consist of osteoporosis, bone resorption, osteonecrosis, and dystrophic soft tissue calcifications (burns).

Inflammatory:
1. rheumatoid arthritis
2. osteomyelitis
3. tuberculosis

Localized osteoporosis is usually the first, although nonspecific, radiographic manifestation
of any inflammatory disease.

Bone infarct and hemorrhage

In their early stages, both bone infarcts and hemorrhages produce localized demineralization. With healing, lesions become calcified and eventually osteosclerotic.

Radiation osteonecrosis (Fig. 1.19)

Radiation changes are dose-related, with a threshold level of 30 Gy and cell death occurring at 50 Gy. Radiographic changes occur one year after radiotherapy at the earliest. They
are initially often predominantly lytic, and progress with time to a mixed lytic and sclerotic
stage.

Tumor (Fig. 1.20)

Osteolytic metastases and multiple myeloma must primarily be considered. Primary bone
tumors (benign or malignant) may present as localized deossification, but only rarely.

(continues on page 14)

Fig. 1.17 Reflex sympathetic dystrophy. Patchy demineralization most severe
near the joints is quite characteristic.

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1 Osteopenia

13

Fig. 1.18 a, b Shoulder-hand syndrome.
Deossification limited to the left shoulder (a)
and hand (b) several weeks following myocardial infarction is characteristic.

a

b

Fig. 1.19 Radiation osteonecrosis. Deossification of the distal
end of the clavicle with endosteal bone resorption is seen 4 years
after irradiation for breast carcinoma.

Fig. 1.20 Multiple myeloma. Demineralization is most pronounced near the joints, as in reflex sympathetic dystrophy in
Fig. 1.17.

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Table 1.2 (Cont.) Differential Diagnosis of Localized Osteopenia
Etiology

Comments

Paget’s disease (lytic phase)
(Fig. 1.21)

Skull: osteoporosis circumscripta. Long bones: usually a well-defined and V- or wedgeshaped area of deossification originating in the subchondral bone of an epiphysis.

Fibrous dysplasia (Fig. 1.22)

Both purely lytic lesions and a homogeneous, “ground glass” appearance occur, besides
predominantly sclerotic manifestations. Cortical thinning and bony expansion is commonly
associated with lytic lesions in tubular bones.

a

b
Fig. 1.21 a, b Paget’s disease. The lytic phase in two different
patients. Relatively well-defined V-or flame-shaped areas of deossification containing strands of increased bony densities in a slightly
expanded shaft are characteristic (a: proximal tibia, b: distal tibia
and fibula).

Fig. 1.22 Fibrous dysplasia. Widening of the humerus, with a
“ground glass” appearance and a few scattered patchy sclerotic
areas, is evident.

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2

Osteosclerosis

Osteosclerosis is defined as an increase in bone density
caused by increased activity of osteoblasts or by osteogenic
or chondrogenic tumor cells forming bone-like tissue. Calcification of tissue other than osteoid within bone is usually
dystrophic in nature and may also increase the bone density
radiographically.
Ossifications within the medullary cavity commonly present as homogeneous, fluffy, cotton-like or cloud-like densities. They most often are caused by bone islands or osteoblastic metastases (Figs. 2.1 and 2.2). Calcifications within
the medullary cavity typically present as punctate, annular,
comma-shaped or shell-like densities and are commonly associated with chondroid matrix tumors and bone infarcts
(Figs. 2.3 and 2.4).
The increase in bone density may be scattered or diffuse.
This distinction appears useful in the differential diagnosis
of osteoblastic reactions, since certain diseases may exclusively present as scattered (solitary or multiple) sclerosis.
Accordingly, the differential diagnosis of these entities will
be discussed separately in Tables 2.1 and 2.2. Table 2.3 lists
sites and commonly used eponyms for idiopathic avascular
necrosis.

Fig. 2.2 Osteoblastic metastasis (breast
carcinoma). An osteoblastic lesion is seen in
the intertrochanteric area.

Fig. 2.1 Bone island. A sclerotic focus is seen in the intertrochanteric area. The lesion depicts both tiny radiating bone spicules in its
periphery and a central radiolucency, both radiographic features
that help to differentiate it from an osteoblastic metastasis.

Fig. 2.3 Enchondroma. An

oblong lesion consisting of
multiple irregular, often punctate calcifications is seen in
the proximal tibia shaft.

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Fig. 2.4 Bone infarct. An oblong radiodense lesion with
shell-like calcifications is seen
in the distal femur shaft.


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Table 2.1

Solitary or Multiple Scattered Osteosclerotic Lesions

Disease

Radiographic Findings

Comments

Bone island (enostosis)
(Fig. 2.5)

Well-circumscribed isolated area of increased density rarely exceeding 1 cm in diameter. A very slow
growth in size is occasionally observed. Margins

demonstrate characteristically tiny spiculations or a
“brush” border. A central radiolucency is occasionally observed. Occur at any location but pelvis and
upper femora appear to be most common locations.

Radionuclide bone imaging is normal.
(DD: Osteoblastic metastases are invariably associated with a markedly increased radionuclide
uptake.)
A large, very dense and structureless bone island
within the medullary cavity is often called enostoma (Fig. 2.6). Without proper clinical history
such a lesion is often indistinguishable from a surgically excised and methylmethacrylate cemented
bone lesion (Fig. 2.7).

Osteopoikilosis
(Fig. 2.8)

Multiple round or ovoid bone densities ranging in
size from 2 mm to 2 cm. May demonstrate a radiolucent center. Can be found in all bones, but
skull, mandible, ribs, sternum, and vertebrae are
only rarely involved. In long bones they are characteristically located in metaphyses and epiphyses,
whereas in the scapula and pelvis they are typically
found around the glenoid fossa and acetabulum,
respectively.

Rare familial disorder not associated with clinical
symptoms and therefore incidentally discovered at
any age. No increased radionuclide uptake is found
in bone scans.

Osteopathia striata
(Fig. 2.9)

Dense longitudinal striations that involve the
metaphyses and may extend into the epiphyses
and diaphyses. In the ilium, the linear densities
radiate from the acetabulum. Vertebral bodies and
skull may also be involved.

Rare and usually asymptomatic bone disorder. Occasionally associated with focal dermal hypoplasia
(Goltz’s syndrome)

Chondrodysplasia
punctata (congenital
stippled epiphyses)
(Fig. 2.10)

Multiple punctate calcifications occurring in the
epiphyses before the normal time of appearance
of the epiphyseal ossification centers.
DD: Zellweger’s cerebrohepatorenal syndrome,
where the stippling is limited to the patella.

Rare genetically heterogeneous epiphyseal dysplasia associated with a broad spectrum of clinical
symptoms. Affected bones may be shortened, or
the disorder may regress and leave no deformities.
The epiphyseal calcifications may disappear by the
age of 3, or may gradually increase in size and
coalesce to form a normal-appearing single ossification center.

Multiple epiphyseal
dysplasia (Fairbank’s

disease)

Irregular mottled calcifications of the epiphyses diagnosed in children and adolescents. Sequelae in
the adult consist of epiphyseal irregularities,
degenerative joint changes, and rarely, asymmetrical shortening of tubular bones.

Can be considered to be the tarda form of
chondrodysplasia punctata.
Cretinism with delayed appearance of stippled and
fragmented epiphyseal ossification centers and
sclerotic metaphyseal bands must be differentiated.

(continues on page 18)

Fig. 2.5 Bone island. Well-circumscribed focus of increased density
with tiny spiculations in its periphery
(“brush” border) is seen in the ilium.

Fig. 2.6 Large bone island
(enostoma). A large, very
dense and structureless lesion
is seen in the proximal
humerus.

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Fig. 2.7 Methylmethacrylate
bone cement. Sequelae of excision with subsequent
cementing of a giant cell
tumor are seen in the distal

femur.