Axial Arthritis
In the appendicular skeleton, one is mostly
concerned with the diarthrodial synovial joints.
While this type of joint is also found in the axial
skeleton (the facet (a.k.a. aphophyseal) joints
and portions of the sacroiliac joints), there are
also many amphiarthrodial joints which are not
synovial (the intervertebral disc joints).
However, there are several structures in the
intervertebral disc joint which are analogous to
structures found in a true synovial joint. The
cartilaginous endplate, the annulus fibrosus, and
the nucleus pulposus are analogous to the
articular cartilage, the joint capsule and the
synovial fluid of the synovial joint.
The different anatomy and physiology of these
joints means that we will see different disorders
affecting this part of the skeleton. However, the
same basic logical principles mentioned in the
last chapter also apply here.
Degenerative disorders
Osteoarthritis
This is, by far, the most common type of arthritis
seen in humans. By definition, osteoarthritis
occurs in a synovial joint. In the spine,
therefore, osteoarthritis occurs in the
apophyseal (facet) joints, the uncovertebral
joints (cervical spine), the costovertebral joints,
and the sacroiliac joints. Osteoarthritis may be
primary or secondary.
marked osteophytosis and joint space narrowing
is noted in the facet joints in this patient with
severe osteoarthritis of the lumbar spine -- the
osteophytosis is causing significant
encroachment on the lateral recesses bilaterally
Degenerative nuclear disease
Another very common disorder is degeneration
of the nucleus pulposus. With age, the nucleus
tends to become more and more dehydrated,
and gradually begins to degenerate. As this
happens, the intervertebral disc height begins to
decrease. When this happens, the altered
pattern of stresses may lead to marginal
osteophytosis adjacent to the affected
endplates. As the disc space decreases in height,
increased stress is also placed on the facet
joints, leading to the frequent association of
osteoarthritis of the facets at the same level.
with increasing age (arrow), progressive
degeneration of the nucleus leads to decreasing
disk space height
Degenerative annular disease
Yet another extremely common degenerative
disorder involves degeneration of the annulus
fibrosus. This leads to marginal osteophytosis at
the endplates, especially in the thoracolumbar
spine in many persons over 50 years of age. In
the literature, this entity has been termed
"spondylosis deformans" or "senile ankylosis".
However, both of these terms tend to make the
disease sound a lot worse than it really is. Using
these terms in a film report can lead to calls
from clinicians wondering just what horrible
disease their patients have. Therefore, I prefer
to state "marginal osteophytes are noted at
multiple disc spaces in the spine" in my
dictations. The clinicians know what I'm
describing and they and their patients are not
unduly frightened by the unfamiliar terminology
used for this very familiar process.
with increasing age (arrow), progressive
degeneration of the annulus leads to increasing
osteophytosis at the disk space margins -- the
height of the disk space is largely preserved
In practice, one often sees evidence of
degeneration of both the annulus and the
nucleus. It usually doesn't make a lot of
difference to the referring clinician which
component of the disk has degenerated.
Therefore, I suggest using the term
"degenerative disk disease" in one's dictations to
refer to these entities.

marked marginal osteophytosis is noted at each
disk space in this patient with predominantly
annular degeneration
disk space narrowing is noted at multiple levels
in this patient with degenerative disk disease --
a thin linear area of lucency in the L4-5 disk
space represents gas in the degenerated disk
Diffuse Idiopathic Skeletal Hyperostosis (DISH)
DISH is an extremely common entity of
unknown etiology, which manifests itself by
ossification of the anterior longitudinal ligament,
which produces large flowing bony excrescences
along the spine, especially the anterior aspect.
Inflammatory spondyloarthropathies
Rheumatoid arthritis
This is a disorder of unknown etiology
characterized by synovial inflammation, pannus
formation, and then destruction of bone and
cartilage.
Ankylosing spondylitis
This chronic inflammatory disorder of unknown
etiology principally affects the axial skeleton.
Alterations occur in synovial and cartilaginous
articulations and in sites of tendon and ligament
attachment to bone. Over 90 % of caucasian
patients with ankylosing spondylitis are HLA-B27
positive.
Crystalline arthritis
Gout
This is the prototypic crystalline arthropathy,
characterized by the deposition of monosodium
urate crystals in the skin, subcutaneous tissues,
and joints. This is most meaningfully classified
as idiopathic gout, encompassing the vast
majority of individuals, or gout associated with
known disorders or enzymatic defects.
Calcium pyrophosphate crystal deposition
disease
Calcium pyrophosphate crystal deposition
disease: a general term for a disorder
characterized by the deposition of calcium
pyrophosphate dihydrate (CPPD) crystals in or
around joints.
Pseudogout: a term applied to one of the
clinical patterns that may be associated with
CPPD crystal deposition disease. This pattern,
characterized by intermittent acute attacks of
arthritis, simulates the findings of gout.
Chondrocalcinosis: a term reserved for
pathologically or radiologically evident
calcification of hyaline articular cartilage or
fibrocartilage. In some cases, this calcification
may not indicate deposits of CPPD crystals but
rather accumulations of some other crystal.
Pyrophosphate arthropathy: a term used to
describe a peculiar pattern of structural joint
damage occurring in CPPD crystal deposition
disease simulating, in many ways, degenerative
joint disease but characterized by distinctive
features.
Hydroxyapatite deposition disease
This is a disorder characterized by recurrent
painful periarticular calcium hydroxyapatite
deposits in tendons and soft tissues.
Psoriatic arthritis
This is a relatively uncommon arthropathy which
occurs in about 2 to 6 % of patients with
psoriasis. Approximately 25 to 60 % of patients
with psoriatic arthritis are HLA-B27 positive.
Reiter's syndrome
Reiter's syndrome is a relatively uncommon
arthropathy of uncertain etiology with the classic
triad of urethritis, arthritis, and conjunctivitis. Of
all of the rheumatic diseases, Reiter's syndrome
is most suspect for an infectious etiology. It
appears likely that the disease can be
transmitted in association with either epidemic
dysentery or sexual intercourse. The syndrome
frequently follows an infection of the bowel or
lower genitourinary tract, and it seems likely
that these sites are the portals of entry for the
causative agent. It has been suggested that the
abnormalities of the vertebral column may be
related to organisms extending directly to the
sacroiliac joints and spine via the prostatic
venous plexus or via the venous plexus of
Batson. Implicated organisms include
pleuropneumonia-like organisms (PPLO), the
Bedsonia group of organisms, and viruses,
although to date, no single agent has been
definitely incriminated in this disease.
Approximately 75 to 96 % of patients with
Reiter's syndrome are HLA-B27 positive.
Enteropathic arthropathy
This arthropathy occurs in about 1 - 26 % of
patients with ulcerative colitis or Crohn's
disease. The relationship between inflammatory
intestinal diseases and arthritis is not fully
understood. Infectious, immunologic, and
genetic etiologies have been advanced.
Approximately 90 % of patients with ulcerative
colitis or Crohn's disease who develop
spondylitis or sacroiliitis are HLA-B27 positive.
2. Radiographic Hallmarks
Osteophytes
In a diarthrodial joint, this is the sine qua non of
osteoarthritis. Osteophytes can be seen in both
primary and secondary osteoarthritis. They can
also be seen at various entheses, often due to
altered or increased stress at the entheses
(traction osteophytes). The traction osteophytes
of degenerative annular disease begin several
millimeters from the edge of the vertebral body,
and tend to be initially oriented horizontally at
their attachment to the vertebral bodies. They
then often curve slightly and may even form a
complete bony bridge across the disc space.
syndesmophytes (arrows) in the spine of a
patient with ankylosing spondylitis
Disc space narrowing
This almost always means degenerative nuclear
disease or infection. These can often be
distinguished by looking at the adjacent
endplates. In degenerative disc disease, the
endplates are often dense, sclerotic, and
associated with osteophytosis. In infection, the
subchondral line of the endplate often becomes
ill-defined and discontinuous.
Bony proliferation
This is a striking feature of the seronegative
spondyloarthropathies, particularly psoriatic
arthritis. This bony proliferation occurs about
erosions, and probably relates to an
exaggerated healing response of the injured
bone. This proliferation may take the form of
irregular excrescences, subperiosteal deposition
of bone, and intra-articular osseous fusion.
bridging osteophytes in the spine of a patient
Erosions
with degenerative disk disease
In general, the presence of erosions bespeaks
Syndesmophytes
some type of inflammatory disease, whether the
Syndesmophytes are generally seen only in the
erosions are due to synovial hypertrophy,
seronegative spondyloarthropathies. These are
crystalline deposits, or infection.
due to inflammation and ossification of the outer
Crystal deposition
fibers of the annulus fibrosus, known as the
In general, this is indicative of one of the
Sharpey's fibers. This is classically seen in
crystalline arthropathies -- either CPPD or
ankylosing spondylitis. In the other seronegative
hydroxyapatite.
spondyloarthropathies, one usually sees
Sclerosis
paravertebral ossification which forms in the
Not an especially specific finding in spinal
paravertebral connective tissue at some distance
arthropathy.
from the spine. In practice, it may be very
Ankylosis
difficult to distinguish osteophytes from
This may occur as a result of many degenerative
syndesmophytes or paravertebral ossification.
and inflammatory processes in their later stages.
Subluxation
Stability of the spine is maintained by the spinal
ligaments, articular capsules, and discs. Any
arthropathy which causes degeneration or
destruction of these structures may lead to
instability of the spine and subluxation in several
locations.
3. Pattern Approach
Osteoarthritis
Osteoarthritis of the spine looks much like
osteoarthritis elsewhere in the body. Any of the
spinal synovial joints can be affected, including
the facet and uncovertebral joints, the
costovertebral joints, and the SI joints. Findings
include osteophytosis, joint space narrowing,
subchondral sclerosis, and subchondral cyst
formation. Besides causing local joint pain, facet
osteoarthritis may cause nerve root
impingement or compression if the osteophytes
are large enough to extend into the lateral
recess of the spinal canal, as shown below.
marked osteophytosis is seen in the spine of a
patient with osteoarthritis of the lumbar facet
joints -- this osteophytosis is extending into the
lateral recesses bilaterally and causing nerve
root compression
Degenerative disc disease
Degeneration of either the nucleus pulposus, the
annulus fibrosus, or both may be present. While
these processes can often be distinguished from
each other, overlap in findings will be seen in
many patients who have both processes
occurring in the same disc.
The key distinguishing characteristic between
these two processes is disc space narrowing. If
present, this is strongly suggestive of
degenerative nuclear disease. This is often
accompanied by endplate sclerosis and mild to
moderate osteophytosis.
intervertebral disc space narrowing, intradiscal
gas, and osteophytosis are noted in this patient
with predominantly degenerative nuclear
disease
On the other hand, degenerative annular disease
is often not associated with significant disc space
narrowing, and the marginal osteophytes seen
with this entity are often much larger than those
seen with degenerative nuclear disease.
extensive osteophytosis is noted in the thoracic
spine in this patient with predominantly
degenerative annular disease
DISH
With DISH, the flowing ossification seen is
usually along the anterior longitudinal ligament.
Although there has been recent speculation that
DISH may be a disorder of vitamin A
metabolism, DISH remains an idiopathic
disorder. As such, it lacks not only a known
specific cause but also a known specific disease
marker (such as monosodium urate crystals in
gout). Therefore, DISH is necessarily a diagnosis
by exclusion. Since DISH is diagnosed on a
morphologic basis alone, there will be of
necessity some overlap between certain cases of
DISH and other disorders with similar
radiographic features, such as ankylosing
spondylitis, and degenerative disc disease. To
help minimize this overlap, certain arbitrary
morphologic criteria have been proposed.
Finding That Distinguishes
Similar Disorders
Them From DISH
Ankylosing SI and facet joints must be
spondylitis normal
Degenerative Disc spaces must be of
nuclear disease normal height
Ossification must be seen
Degenerative
along four contiguous
annular disease
vertebral bodies
Since we often don't have any specific therapy
for DISH, is there any reason to try to
distinguish it from all of these other disorders? I
feel that there is. If for no other reason,
knowing the name of a disease allows one to be
much more precise in giving a prognosis to a
patient. Knowledge of the presence of DISH may
alter therapy for other disorders. For example,
DISH patients are prone to heterotopic bone
formation in surgical sites. Because of this,
some orthopedic surgeons will prophylactically
treat DISH patients with radiation or drug
therapy prior to performing a total joint
arthroplasty, in an attempt to prevent or
diminish the development of heterotopic bone
formation after surgery.
prominent, flowing ossification is noted along
the anterior margin of the cervical spine in this
patient with DISH -- it is easy to see why such
patients often complain of dysphagia
flowing ossification is noted along the anterior
margin of the thoracic and lumbar spine in these
patients with DISH -- note that the disk spaces
are preserved and that at least four contiguous
bodies are involved
Ankylosing spondylitis
Ankylosing spondylitis affects synovial and
cartilaginous joints as well as sites of tendon
and ligament attachment to bone (entheses). An
overwhelming predilection exists for involvement
of the axial skeleton, especially the sacroiliac,
apophyseal, discovertebral, and costovertebral
articulations. Classically, changes are initially
noted in the sacroiliac joints and next appear at
the thoracolumbar and lumbosacral junctions.
With disease chronicity, the remainder of the
vertebrae may become involved. However, this
characteristic pattern of spinal ascent is by no
means invariable; it may occur slowly or rapidly,
and is less frequent in spondylitis accompanying
psoriasis and Reiter's disease.
Sacroiliitis is the hallmark of ankylosing
spondylitis. It occurs early in the course of the
disease. Although an asymmetric or unilateral
distribution can be evident on initial radiographic
examination, roentgenographic changes at later
stages of the disease are almost invariably
bilateral and symmetric in distribution. This
symmetric pattern is an important diagnostic
clue in this disease and may permit it
differentiation from other disorders that affect
the sacroiliac articulation, such as RA, psoriasis,
Reiter's syndrome, and infection. Changes in the
SI joint occur in both the synovial and
ligamentous (superior) portions, and
predominate on the iliac side, for reasons that
are obscure.
bilateral erosions and sclerosis are noted in the
SI joints of this patient with ankylosing
spondylitis
The classic histologic descriptions of synovial
joint alterations in ankylosing spondylitis stress
that the synovitis is similar or identical to that in
rheumatoid arthritis. Indeed, ankylosing
spondylitis was once called rheumatoid
spondylitis, under the impression that
ankylosing spondylitis was just a variant of
rheumatoid arthritis. Further research into this
entity revealed enough clinical and
immunological differences between the two
entities to warrant calling it a disease of its own.
In general, the inflammatory process in
ankylosing spondylitis is more discrete and of
lower intensity that in rheumatoid arthritis.
erosions are noted in the lumbar facet joints of
this patient with ankylosing spondylitis
The characteristic radiographic features of
ankylosing spondylitis include erosions,
sclerosis, syndesmophytosis, and ankylosis.
Rheumatoid arthritis
As mentioned above, the histological changes
noted classically in rheumatoid arthritis are
similar or identical to those of ankylosing
spondylitis. However, the general pattern of
distribution of these changes are usually quite
distinct from that of ankylosing spondylitis. For
example, rheumatoid arthritis predominantly
involves the cervical spine, with apophyseal joint
erosion and malalignment, intervertebral disc
space narrowing with endplate sclerosis and
without osteophytes, and with multiple
subluxations, especially at the atlanto-axial
junction. Abnormalities of the thoracolumbar
spine and sacroiliac joints are infrequent and
less prominent than those of ankylosing
spondylitis.
the dens is eroded in this patient with
rheumatoid arthritis -- a mass of pannus is
noted behind the dens and impinging on the
thecal sac and cord in these T1- and T2-
weighted MR images
Other helpful differential findings are the
absence of osteoporosis and the presence of
bony proliferation and intraarticular bony
ankylosis in the seronegative
spondyloarthropathies.
CPPD crystal deposition disease
The spine is frequently involved in CPPD crystal
deposition disease.
Intervertebral discal calcifications are frequent in
the outer annular fibers, and may mimic early
syndesmophytes of ankylosing spondylitis,
because of their vertical orientation and slender
appearance. These annular calcifications may be
associated with back pain. Disc space narrowing
is common in CPPD crystal deposition disease,
and may be extensive, widespread, and
associated with considerable vertebral sclerosis.
However, the nucleus pulposus is not commonly
calcified. Calcification of ligamentum flavum may
also be noted. Occasionally, destructive
abnormalities of cervical spine are present.
Chondrocalcinosis is only infrequently seen in
the sacroiliac joints, but is very common in the
fibrocartilaginous joint of the pubic symphysis.
Gout
Spinal manifestations of gout are extremely
uncommon, and documented urate deposition in
the spine is exceedingly rare. When seen, spinal
gout may manifest as erosions of the synovial
joints or endplates, and disc space narrowing
may be present.
The incidence of gout in the sacroiliac joint has
been reported at 7 - 17 %, although many of
the changes ascribed to gout in the earlier
literature were probably mimicked in these
reports by the changes of osteoarthritis.
Sacroiliac joint involvement is seen more
frequently with early onset disease, and large
cystic areas of erosion in ilium and sacrum are
the most specific findings of gout in these joints.
Hydroxyapatite crystal deposition disease
Hydroxyapatite crystal deposition disease is
most commonly seen about the shoulder.
However, it may also occur within the longus
colli muscle, which is the principal flexor of the
cervical spine. Tendinitis in this region may
result in acute neck and occipital pain, rigidity,
and dysphagia. Calcifications tend to occur
particularly in the superolateral group of the
longus colli. The typical radiographic findings of
this disorder consist of prevertebral soft tissue
swelling in upper cervical region, as well as
amorphous calcification, usually anterior to C-2,
and just below the anterior arch of C-1.
Resorption of this calcification and soft tissue
swelling is common, and it may disappear
completely in 1 to 2 weeks.
Psoriatic arthritis
About 30 to 50 % of patients with psoriatic
arthritis develop sacroiliac joint changes
radiographically. Bilateral sacroiliac joint
abnormalities are much more frequent than
unilateral changes, and although asymmetric
findings may be apparent, symmetric
abnormalities predominate. Radiographic
sacroiliac joint changes include erosions and
sclerosis, predominantly on the iliac side, and
widening of the articular space. Although
significant joint space diminution and bony
ankylosis can occur, the incidence of these
findings, particularly ankylosis, is less than that
of classic ankylosing spondylitis or the
spondylitis associated with inflammatory bowel
disease. Sacroiliitis may appear without
spondylitis, just as spondylitis may appear
without sacroiliitis.
As in Reiter's syndrome, paravertebral
ossification about the lower thoracic and upper
lumbar segments can occur in psoriatic arthritis,
and it may represent an early manifestation of
the disease. Such ossification appears as a thick
and fluffy or thin and curvilinear radiodense
region on one side of the spine, paralleling the
lateral surface of the vertebral bodies and the
intervertebral discs. Occasionally, slender,
centrally located, and symmetric spinal
outgrowths in psoriasis are identical in
appearance to the syndesmophytes of
ankylosing spondylitis. However, the greater
size, the unilateral or asymmetric distribution,
and the location farther away from the vertebral
column are features that distinguish
paravertebral ossification from the typical
syndesmophytosis of ankylosing spondylitis or
the spondylitis of inflammatory bowel disease.
In addition to the pattern and distribution of
bony outgrowths, there are other features of
psoriatic spondylitis that differ from those in
classic ankylosing spondylitis. Osteitis and
squaring of the anterior surfaces of the vertebral
bodies are relatively infrequent in psoriasis.
Although apophyseal joint space narrowing,
sclerosis and bony ankylosis may be seen, the
prevalence of these findings is much less than
that in ankylosing spondylitis.
Cervical spine abnormalities may be striking in
psoriatic arthritis, including apophyseal joint
space narrowing and sclerosis, osseous
irregularity at the discovertebral joint, and
extensive proliferation along the anterior surface
of the spine. Atlanto-axial subluxation can also
be evident (in one series up to 45 % of patients
with psoriatic spondylitis).
Reiter's syndrome
Reiter's syndrome is associated with an
asymmetric arthritis of the lower extremity,
sacroiliitis, and, less commonly, spondylitis.
Although its general features resemble those of
ankylosing spondylitis and psoriatic arthritis,
Reiter's syndrome possess a sufficiently
characteristic articular distribution to allow
accurate diagnosis.
Ankylosing spondylitis has a similar axial skeletal
distribution (although cervical changes are more
frequent in ankylosing spondylitis), but
significant peripheral articular changes are more
frequent.
Psoriatic arthritis may lead to considerable
alterations in the articulations of both the
appendicular and the axial skeleton. However, in
psoriasis, widespread involvement of the upper
extremity may be apparent, and distal
interphalangeal joint abnormalities in both upper
and lower extremities are common. The
sacroiliac and spinal changes of Reiter's
syndrome are virtually identical to those of
psoriasis, although the incidence and severity of
these abnormalities and the tendency to involve
the cervical spine are greater in psoriasis.
sclerosis and ill-definition of both SI joints is
noted in this patient with Reiter's syndrome
bony proliferation (arrows) is noted along the
anterior margin of the lumbar spine in this
patient with Reiter's syndrome
Enteropathic arthropathy
The spondylitis and sacroiliitis of inflammatory
bowel disease are identical to those of classic
ankylosing spondylitis. The history of
inflammatory bowel disease can sometimes help
to distinguish these entities, although spondylitis
in ulcerative colitis is poorly correlated with
activity of the bowel disease. In ulcerative
colitis, spinal abnormalities may become
manifest prior to, at the same time as, or
following the onset of intestinal changes. In fact,
spondylitis most commonly precedes the onset
of colitis and may progress relentlessly without
relation to exacerbation, remission, or treatment
of the bowel disease. In Crohn's disease, the
joint abnormalities tend to occur simultaneously
with the bowel disease.
Peripheral joint abnormalities tend to occur
much more frequently with enteropathic
arthropathy than with ankylosing spondylitis.
When they do occur, they are usually self
limited, and rarely cause lasting deformity of the
joint. However, in ankylosing spondylitis, the
peripheral joint findings typically include joint
space narrowing, osseous erosions, cysts, and
bony proliferation, which may help in
distinguishing these entities.
4. Demographics
All of the entities described in this section on
axial arthropathies can occur in the young or the
old, and in men or women. However, just as in
the appendicular arthropathies, there are certain
trends in the distribution of these disorders that
may sometimes be helpful in refining one's
differential diagnosis. The following tables show
some of these trends. As with the appendicular
arthropathies, other demographic features such
as home location, occupation, and ethnic
subtype may occasionally be of help.
Age
Age of Disorder
Age Group
Onset
Juvenile chronic
Young (< 20 arthritis
< 20 years
years) Septic arthritis
 Ankylosing disorders. Even though over 90 different
onset 15 - spondylitis rheumatic diseases are recognized by the
35 years Reiter's American College of Rheumatology, only three
entities are commonly seen in most clinical
radiology practices, even including those located
Enteropathic in large tertiary medical centers. Osteoarthritis
Middle (> 20 Young
arthropathies (a.k.a. degenerative joint disease) is the most
years) adults
commonly seen form of appendicular arthritis.
The other two commonly seen arthropathies are
Rheumatoid
rheumatoid arthritis and calcium pyrophosphate
25 - 55 arthritis
dihydrate (CPPD) deposition disease. Less
years Psoriatic arthritis
common arthropathies that may manifest
radiographic findings in the appendicular
Osteoarthritis skeleton include septic arthritis, and gout. Most
Older patients other appendicular arthropathies are seen only
> 55 years DISH
(> 55 years) rarely.
CPPD
2. Radiographic Hallmarks
Arthropathies with Male Predominance In George Orwell's Animal Farm, it is stated that
Disorder male:female ratio "All animals are equal. But some animals are
more equal than others." This principle is
Ankylosing spondylitis 4:1 to 10:1 manifested in the appendicular arthropathies,
where some radiographic findings are quite
2:1 to 3:1, but specific and can quickly lead one to the correct
Psoriatic
controversial diagnosis. Other findings are less specific and
Reiter's 5:1 to 50:1 are usually unhelpful in ordering one's
differential diagnosis.
Gout 20:1 In a diarthrodial joint, osteophytes are the sine
qua non of osteoarthritis. Osteophytes can be
DISH 3:2
seen in both primary and secondary
CPPD 1:1 osteoarthritis.

Primary osteoarthritis
(< 45 years)
Enteropathic
arthropathy
Ulcerative colitis 4:1
Crohn's disease 1:1
Arthropathies with Female Predominance
Disorder female:male ratio
Rheumatoid Arthritis 2:1 to 3:1
marked osteophytosis (arrows) is seen in the
Primary osteoarthritis DIP and PIP joints in these fingers
(> 45 years)
CPPD 1:1
5. The law of parsimony
As in the appendicular arthropathies, a patient
may have more than one arthropathy going on
in a given joint. Again, this is most commonly
due to secondary osteoarthritis due to some
other arthropathy, although other unusual
combinations of arthropathies may be seen. This
principle can sometimes help to clarify what
otherwise might be a confusing radiographic
picture. osteophytosis (arrow) is noted at the articular
Appendicular Arthritis margin of the femoral head
1. Sutton's Law Osteophytes can also be seen at various
This law has been ascribed to Willie Sutton, a entheses (sites of tendinous or ligamentous
famous bank robber. When asked why he robbed attachment to bone), often due to altered or
banks, he reportedly said, "Because that's where increased stress there.
the money is." In the radiographic evaluation of In general, the presence of erosions bespeaks
appendicular arthropathies, the "money" is some type of inflammatory disease, whether the
generally in a relatively small handful of
erosions are due to synovial hypertrophy,
crystalline deposits, or infection.
In rheumatoid arthritis, the erosions follow the
development of an inflammatory proliferation of
the synovium, called pannus. As this pannus
increases in amount, it begins to cause erosions
of the chondral surface.
As the pannus increases further in amount, one
begins to see erosions at the periarticular "bare"
areas. These "bare" areas refer to bone within
the synovial space which is not covered by
articular cartilage. The articular cartilage tends
to protect the bone that it covers. The marginal
"bare" areas are not covered by cartilage, and
the earliest erosions of rheumatoid arthritis are
seen here.
erosions (arrows) are noted in the periarticular
areas of the toes in this patient with rheumatoid
arthritis
multiple erosions and marked joint space
narrowing are noted in a pancarpal distribution
in this patient with rheumatoid arthritis
erosions (arrows) are noted at the articular
margins of the tibia in this patient with juvenile
chronic arthritis
If the inflammation proceeds unchecked, the
erosions of the bone and the cartilage may
become profound, and the joint may finally
undergo fibrous ankylosis.
The presence of crystal deposits
(chondrocalcinosis or tophi) indicates one of the
crystalline arthropathies. In calcium
pyrophosphate dyhidrate depostition (CPPD)
disease, the most common site of radiographic
calcifications is in fibrocartilage and hyaline
articular cartilage (chondrocalcinosis). However,
calcifications may also be seen in the joint
capsule or synovial membrane.
calcification may be seen at several sites about a
joint in CPPD
chondrocalcinosis is seen in the triangular
fibrocartilage of this wrist
chondrocalcinosis is seen in both the
fibrocartilage of the menisci and in the hyaline
articular cartilage of this knee
In gout, erosions are caused by tophi. These
tophi may be either intra- or extra-articular in
location. Calcifications are occasionally seen in
tophi. The erosions of gout may appear very
similar to those seen in rheumatoid arthritis.
However, in gout, there tends to be early
sparing of the articular cartilage between the
erosions, while the cartilage is thinned much
earlier in the course of rheumatoid arthritis.
 joint compartments of the wrist -- CMC (first
carpometacarpal), CCMC (common
carpometacarpal), ST (scaphotrapezial), MC
(midcarpal), RC (radiocarpal), and DRUJ (distal
radioulnar joint)
a gouty erosion (arrow) is noted along the
medial margin of the first metatarsal head in
this patient with gout -- relative sparing of the
articular cartilage is also noted
Other findings, such as joint space narrowing,
subchondral cyst formation, sclerosis, ankylosis,
or subluxation are not especially specific and
may occur in a wide variety of degenerative or
inflammatory disorders in the appendicular
skeleton. It is important to describe these
findings, as they tell us a lot about the severity typical distribution of arthritis in the wrists
of the patient's disease -- it's just that they
don't tell us a whole lot about what specific
disease is causing them.
3. Pattern Approach
It would be nice if one could start with a few
basic pathophysiological axioms, and from these
first principles go on to deduce the characteristic
sites of joint involvement of the various
appendicular arthropathies. Unfortunately, such
principles remain obscure, forcing one to
memorize empirical patterns. However, once
learned, these patterns can be helpful in typical distribution of arthritis in the knees
ordering the differential diagnosis. Although
such patterns have been described for most of
the appendicular joints (Resnick, 1995), the
most specific of these patterns of joint
involvement are seen in the hands and wrists.
Less specific patterns are seen in the hips and
knees.

typical distribution of arthritis in the hips

Any joint in the body can be affected by
secondary osteoarthritis due to trauma, infection
or another arthropathy. However, the findings of
primary (idiopathic) osteoarthritis are usually
seen in the distal interphalangeal (DIP) joints of
the hand, and the first carpometacarpal joint
and scaphotrapezial joint of the wrist. The
proximal interphalangeal (PIP) joints may
typical distribution of arthritis in the hands
occasionally be affected. Rheumatoid
arthritis(RA)tends to involve the PIP and
metacarpophalangeal (MCP) joints of the hand
and all of the major joint compartments of the
wrist (pancarpal involvement). CPPD deposition
disease usually initially affects the radiocarpal
(RC) joint in the wrist, but may also involve the
MCP joints of the hand.
4. Demographics
Age and gender may occasionally be useful in
narrowing the differential diagnosis of the
appendicular arthropathies. For example, the
most common arthropathies in children are
juvenile chronic arthritis and septic arthritis,
while entities such as rheumatoid arthritis,
osteoarthritis and CPPD arthropathy are
generally seen in older adults. CPPD arthropathy
affects both genders equally. Rheumatoid
arthritis has a moderate female predominance,
as does osteoarthritis in the older age group.
Gout, on the other hand, has a moderate to
strong male predominance.
Other demographic factors, such as home
location, occupation and even ethnic subtype
can occasionally be helpful in steering the
differential toward or away from certain disease
entities.
5. The Law of Parsimony
In the first two years of medical school, one is
taught to take historical points and physical
findings and to put them together into one
diagnosis which explains everything (the law of
parsimony). However, once one reaches the
ward rotations and opens a patient's chart to the
problem list, one sees that most real patients
have several disorders going on simultaneously.
By the time one gets out of medical school, into
radiology, and begins to interpret joint films, this
lesson often seems to have been lost. In real
life, patients often have more than one
arthropathy. This is most commonly seen in
patients with secondary osteoarthritis
superimposed upon some other arthropathy.
Virtually any arthropathy which causes cartilage
loss can lead to secondary osteoarthritis, with all
of the classic signs of osteoarthritis, including
osteophytosis. In fact, in certain patients, the
changes from the primary arthropathy may be
significantly obscured by the secondary
osteoarthritic changes. A clue that this is
happening is that the most distinctive sign of
osteoarthritis, osteophytosis, is often fairly
minimal compared to other findings such as joint
space narrowing or subchondral sclerosis. In
fact, this is a very common presentation of
rheumatoid arthritis of the knee: marked joint
space narrowing and subchondral sclerosis, but
no evident erosions, and only minimal
osteophytosis. In primary osteoarthritis, on the
other hand, marked joint space narrowing is
usually accompanied by moderate or marked
osteophytosis.
Other combinations of arthropathies are
possible, such as gout and CPPD, gout and RA,
RA and DISH (RADISH), etc. Therefore, when
apparently contradictory findings are noted,
remember that the law of parsimony is often
broken.
Conclusion
The five simple principles listed above are
neither absolute nor comprehensive, and they
should not be followed dogmatically. Relying
solely on them for the diagnosis of arthritis
would be like using only the rule "buy low, sell
high" to seek wealth. However, these principles
form an effective framework for the diagnosis of
most of the cases of appendicular arthropathy
which one actually sees in a clinical radiology
practice, and can be very helpful in elucidating
the cause of even radiographically complex
arthropathies.
Lucent Bone Lesions
Mnemonic = FOGMACHINES
Differential Diagnosis of Solitary Lucent
Bone Lesions
• Fibrous Dysplasia
• Osteoblastoma
• Giant Cell Tumor
• Metastasis / Myeloma
• Aneurysmal Bone Cyst
• Chondroblastoma / Chondromyxoid
Fibroma
• Hyperparathyroidism (brown tumors) /
Hemangioma
• Infection
• Non-ossifying Fibroma
• Eosinophilic Granuloma / Enchondroma
• Solitary Bone Cyst
This is a fairly long differential diagnosis.
However, it is one that you must learn. I still run
through it every time I see one of these lesions,
just to make sure that I consider all of the
important possibilities.
The discussion that follows will dwell almost
totally on the plain radiographic findings of these
lesions. CT and MRI are wonderful tools for
tumor workups, but they are fairly non-specific.
Their place in the workup is to tell us where the
lesion is: what its extent is; whether there are
any metastases (either in the same bone or
elsewhere); and whether an adjacent joint,
nerve or blood vessel is involved. However, to
tell us what a lesion is, the plain radiograph is
still supreme. We've been looking at the darned
things for almost a century now, and the plain
film findings of most bone tumors are fairly well
known. Plain films are not terribly sensitive, but
they do have a decent specificity. Therefore, any
workup of a bone tumor should start with a good
set of plain films.
Age
Patient age is a very important bit of knowledge
to have in the workup of a tumor. According to
Edeiken, about 80% of malignant tumors can be
correctly diagnosed on the basis of age alone.
From a study of the age prevalence of 4,000
malignant bone tumors, he gives the following
table:
Age vs. Malignant Tumor Type
AGE
TUMOR
(years)
1 neuroblastoma
1 - 10 Ewing's of tubular bones
10 - 30 osteosarcoma, Ewing's of flat bones
 reticulum cell sarcoma (Primary producing a sclerotic and usually distinct margin
histiocytic lymphoma), fibrosarcoma, around the lesion. If process grows more rapidly,
30 - 40 the bone may only have time to retreat before
parosteal osteosarcoma, malignant
giant cell tumor, lymphoma the lesion, and not have time to lay down this
sclerotic rim. Solitary lucent lesions in bone with
metastatic carcinoma, multiple a distinct margin are generally called
40 +
myeloma, chondrosarcoma "geographic" lesions, whether or not they have a
Size sclerotic rim.
What does the size of a lesion tell us?
Unfortunately, not a whole lot about the
histological type of lesion that we are dealing
with. However, describing the size of a lesion is
part of another important aspect of tumor
management: pretreatment staging of the
extent of the lesion.
Surgery is the preferred treatment for many
lesions in this category. The surgeon wants to
know where to cut so as to remove all of the
lesion, along with an area of normal tissue on all
margins of the tumor. Lesion size as measured
on plain films will not tell us this accurately -- if geographic lesion with geographic lesion with
anything, it tends to greatly underestimate the ill-defined rim well-defined rim
extent of the lesion. However, it provides a If the lesion grows more rapidly still, there may
convenient first-order approximation of the not be time for the bone to retreat in an orderly
extent (a lower bound on its size) while the manner, and the margin may become ill-defined.
early workup is being arranged. Definitive Rather than a single discrete lesion, we may see
assessment of the pretreatment extent of a several ill-defined foci of lucency. This has been
lesion will require MR or CT. termed a "moth-eaten" pattern.
Margins
This is one of the most important things that
you can determine about a solitary, lucent,
expansile lesion of bone. Why is this? Because,
this is the finding that will give you your best
shot at determining the biological activity of the
lesion (how fast is it growing?). This is
important, because in general, the faster a
process grows, the more likely it is to be
malignant.
So, how can we determine biological activity
from the margin of the lesion? The answer is
bone response. Bone is sensitive to a variety of a "moth-eaten" lesion
stimuli, and generally responds to one of the If, alas, the process grows more rapidly still,
processes in FOGMACHINES by either removing then the bone's retreat may become disorderly
bone or creating bone. That's right! The bone indeed. Continuing this battlefield analogy, the
itself does the removing or creating of bone - boundary between normal and abnormal bone
not the disorder involving the bone. At the AFIP, may be lost altogether, with only a very ill-
they are fond of saying that the only things that defined pattern of lucency seen, caused by
can remove bone are osteoclasts and orthopedic many small, irregular holes in the bone, left
surgeons. I agree with this rule, but would also behind by osteoclasts. This is an extremely
add talented amateurs to the list (lawnmower aggressive pattern, sometimes called a
and saw accidents, auto crashes, blast injuries, "permeative" pattern.
and animal bites are favored mechanisms of
bone removal by amateurs -- professionals
prefer saws, drills, and osteotomes and confine
their efforts to operating rooms). For this
reason, the term "expansile lesion" is a bit of a
misnomer, since the lesion itself is not
expanding the bone. The bone is remodeling
itself in response to the stimulus of the lesion.
The other thing to know about bone response is
that while it is certain, it is rather slow. If a
lesion is growing slowly, then the bone will have
plenty of time to retreat from the lesion,
removing some bone around the lesion, but also permeative pattern normal bone
laying down new bone around the margins of
the lesion. This generally has the effect of
The presence of a permeative pattern usually
means that the patient either has an aggressive
infection or a malignant tumor. The most
common malignancies that give this pattern are
metastases, myeloma, primary histiocytic
lymphoma, and Ewing's sarcoma. These lesions
are sometimes referred to as "round cell lesions"
due to the small, dark, round cells that they
display to the pathologist.
Matrix
What is matrix, anyway? It is stuff produced by
osteoblasts and chondroblasts that eventually
becomes, respectively, normal bone and
cartilage. Bone tumors form matrix just as a
normal bone does, but sometimes in greater
quantity. Also, matrix produced by tumors is
usually quite abnormal, and does not ossify
properly. Why do we look for tumor matrix?
Because, it helps us to give a bone tumor a
rough histological classification into one of three
categories: cartilage-producing, bone-producing
or other. Cartilaginous tumors (enchondroma,
chondrosarcoma, chondromyxoid fibroma, etc.)
will tend to produce cartilaginous matrix, while
tumors from the osteoid series (osteoma,
osteoblastoma, osteosarcoma, etc.) will tend to
produce osseous matrix. In order to see matrix
on plain radiographs, it has to calcify. Chondroid
matrix, for example tends to produce small
punctate or swirled areas of calcification.
Adjectives applied to this cartilaginous matrix
include "popcorn-like", "curvilinear", or
"speckled". Osseous matrix tends to be dense
and confluent, and invokes descriptive terms like
"cloud-like" or "mashed potatoes". Other lesions
tend to produce little or no calcification in their
matrix (fibrous dysplasia, fibrosarcoma,
malignant fibrous histiocytoma, solitary bone
cyst, etc.). Although the term "ground-glass"
has been applied to this appearance of matrix, I
think that it is a bit confusing, since a fogged
film with no diagnostic information on it has a
ground-glass appearance also. If I don't see any
definite calcified matrix in a lesion, I prefer to
just say that instead.
Location
Most expansile, lucent lesions are located in the
medullary space of the bone. However, we can
further define the location of the lesion by noting
its relationship to the physis. Many lesions tend
to occur in a "favorite" part of the bone. The
favored locations are listed in the figure below.
figure after Madewell, et al 1981
Epiphysis
Very few lesions tend to arise in the epiphysis.
Chondroblastoma is one of the very few tumors
that arise here before the physis closes.
Osteomyelitis can also arise in the epiphysis.
Several entities can spread across the physis.
Osteomyelitis is a classic example of this.
Although the dogma for years has been that
malignancies such as osteosarcoma and Ewing's
tumor rarely cross the physis, more recent
experience with MRI has shown this to be
untrue. With very sensitive pulse sequences
such as STIR (short-tau inversion recovery),
subtle extension across the physeal plate may
be seen not uncommonly.
After the plate closes, the physis ceases to be an
anatomic barrier to disease, and a variety of
lesions can be seen involving the epiphyseal
area, such as giant cell tumor, enchondroma or
aneurysmal bone cyst. Helpful tips in steering
the differential diagnosis among these entities
include the facts that most enchondromas will
exhibit chondroid matrix, most giant cell tumors
will abut an articular margin, and most
aneurysmal bone cysts appear, well,
"aneurysmal" or expansile. It was once thought
that aggressive tumors, such as Ewing's tumor
and osteosarcoma tended to "respect" the
physeal plate and only rarely cross it. However,
more recent studies (Panuel, Norton) of the
behavior of such tumors with sensitive MR pulse
sequences show that osteosarcomas may cross
the plate into the epiphysis in 70 - 80 % of
cases and Ewing's tumor in about 20 %.
Metaphysis
This is the fastest growing area of a bone, and
also the most likely area for a primary neoplasm
to arise. This is especially true in the distal
femur and proximal tibia, which are the fastest
growing metaphyseal areas in the skeleton. The
metaphysis also has the best blood supply of the
bone, so entities such as infection or metastasis
will commonly be seen in this area as well. In
general, most of the entities in FOGMACHINES
(with the exception of chondroblastoma) will be
most commonly seen in the metaphyseal area of
a given bone.
Diaphysis
Most of the entities in FOGMACHINES can also
appear in the diaphysis, although with less
frequency. Notable exceptions are:
chondroblastoma, which almost always occurs in
an epiphysis or epiphyseal equivalent (most
apophyses, the patella and the calcaneus); giant
cell tumor, which almost always occurs in an
apophysis or in the bone adjacent to a join
space; osteoblastoma, which usually occurs in
the posterior elements of the spine; and
aneurysmal bone cyst, which is usually
metaphyseal in location.
Periosteal Reaction
Periosteal reaction is an important finding to
note in the workup of bone tumors. However, it
also occurs due to several other processes
besides tumors. Therefore, I have given
periosteal reaction a chapter all to itself. Please
refer to this chapter on periosteal reaction for a
discussion of how it relates to bone tumors.
Multiplicity
So, what do you do if the patient has multiple
lucent lesions? Well, you go through pretty much
the same thought processes that you went
through for a solitary lesion. The main thing that
is different is the differential diagnosis that you
use. A lot of the entities in FOGMACHINES don't
really make sense as a cause of multiple lucent
lesions. However, some of them do. It turns out
that one can simply trim out the entities that
don't make sense and what's left works just fine
for multiple lesions. Thus, our differential
reduces like this:
Differential Diagnosis of Multiple Lucent
Bone Lesions
Mnemonic = FOGMACHINES --> FEMHI
• Fibrous Dysplasia
• Metastasis / Myeloma
• Hyperparathyroidism (brown tumors) /
Hemangioma
• Infection
• Eosinophilic Granuloma / Enchondroma
This leaves the letters FMHIE as our differential
for multiple lucent lesions. Try as I might, I still
haven't been able to come up with any kind of
decent word out of these letters. Clyde Helms
orders them as FEMHI, and you can make up
your own order if you like. If you do come up
with a real word in English or some other
language out of these five letters, tell me what it
is and I will buy you a taco.
Wise Sayings About Solitary Lucent Lesions
Sometimes, all the logical principles that you
have at your disposal don't seem to help very
much, and one must fall back on some of the
empirical maxims that musculoskeletal
radiologists have accumulated over the years.
Here are a few of the ones I have used over the
years.
1. With a long lesion in a long bone, think
of fibrous dysplasia.
2. Simple cyst, enchondroma, and fibrous
dysplasia can mimic each other and can
be hard to distinguish. Thus, when you
think of one of these three entities, also
think of the other two.
3. Giant cell tumors nearly always occur
near a joint surface.
4. Certain bones in the body can be
considered "epiphyseal equivalents" for
purposes of differential diagnosis.
These include the patella, the
calcaneus, and most apophyses.
Therefore, for lucent lesions in these
areas, one should include the classic
epiphyseal entities such as
chondroblastoma, giant cell tumors and
aneurysmal bone cysts.
5. Lucent lesions of the sternum should be
considered malignant until proven
otherwise (Helms CA, personal
communication, 1983).
6. Keep in mind that the classic
descriptions of bone tumors that you
spend so much time studying are for
untreated lesions. What kind of lesions
do radiologists spend most of their time
looking at? Treated lesions -- treated
with surgery, chemotherapy,
cryotherapy and radiation therapy. In
surgically treated lesions, besides
simple resection of the lesion, one may
also see replacement by a metal
prosthesis, an allograft, or other forms
of bone grafting. In short, you won't
see the "classic" appearance of a lesion
for very long in a given patient. When
the patient first presents to you, you
may not even have any history of these
prior interventions, so you will just
have to remember this phenomenon.
Also, any given film that you see of a
patient is just one frame out of a long
documentary movie about that patient
-- movies change. Remember this
Sclerotic Lesions of Bone
What does it mean that a lesion is sclerotic?
Well, generally, it means that it is due to a fairly
slow-growing process. Bone reacts to its
environment in two ways -- either by removing
some of itself or by creating more of itself. If the
disorder it is reacting to is rapidly progressive,
there may only be time for retreat (defense). If
the process is slower growing, then the bone
may have time to mount an offense and try to
form a sclerotic area around the offender.
How should one approach sclerotic bone
disease? I think that the best way is to start
with a good differential diagnosis for sclerotic
bones. One can then apply various features of
the lesions to this differential, and exclude some
things, elevate some things, and downgrade
others in the differential.
Let's apply the good old universal differential
diagnosis to sclerotic bone lesions.
Mnemonic = VINDICATE
Generic Differential Diagnosis of Sclerotic
Bone Lesions
• Vascular
 o hemangiomas o fracture (stress)
o infarct • Endocrine/Metabolic
• Infection o Paget's disease
o chronic osteomyelitis As you can see, by just dropping the items that
• Neoplasm tend to cause generalized sclerosis, we have
generated a fairly good differential for focal
o primary lesions. The differential for multifocal lesions
 osteoma happens to be identical to that for focal lesions.
 osteosarcoma Differential Diagnosis of Diffuse Sclerotic
o metastatic Bone Lesions
 prostate • Vascular
 breast
o infarct (e.g. sickle cell)
 other • Neoplasm

• Drugs
o metastatic
o Vitamin D  prostate
o fluoride  breast
• Inflammatory/Idiopathic  other
• Congenital • Drugs
o bone islands o Vitamin D
o osteopoikilosis o fluoride
o osteopetrosis • Congenital
o pyknodysostosis o osteopetrosis
• Autoimmune o pyknodysostosis
• Trauma • Endocrine/Metabolic
o fracture (stress) o hyperparathyroidism
You may have been surprised to see metastatic
• Endocrine/Metabolic
disease listed as a leading cause for diffuse
o hyperparathyroidism sclerotic bones. It is true that the usual
o Paget's disease appearance of skeletal metastases is that of
One of the first things you should notice about focal lesions -- diffuse sclerosis occurs in only a
sclerotic bone lesions is whether they are single small fraction of cases of skeletal metastases.
and focal, multifocal, or diffuse. You can then However, cancers that metastasize to bone are
customize the above differential for whichever very common. The lesson here is that when we
pattern of sclerosis that you see. Generally, this are dealing with a very common disorder, even
just follows common sense -- some lesions its less common presentations will be seen
should logically be expected to be focal, others commonly.
multifocal, and yet others diffuse or systemic.
For example:
Differential Diagnosis of Focal or Multifocal
Sclerotic Bone Lesions
• Vascular
o hemangiomas
o infarct
• Infection
o chronic osteomyelitis
• Neoplasm
o primary diffuse sclerotic metastases to the pelvis,
 osteoma sacrum and femurs
Wise Sayings About Sclerotic Lesions
 osteosarcoma There are a number of other helpful findings you
o metastatic can look for that can help you to cone in on or
 prostate away from specific entities in one of these
 breast differential lists.
1. Most cases of chronic osteomyelitis look
 other
pretty nonspecific. However, if one sees
• Congenital sinus tracts associated with a sclerotic
o bone islands area, one should strongly consider
o osteopoikilosis osteomyelitis.
2. Diffuse skeletal infarcts can be a
• Trauma
common cause of diffuse skeletal
 sclerosis. In fact, in areas where sickle
cell disease is common, this may be the
leading cause of diffuse sclerotic bones.
When you are considering
osteonecrosis in your differential
diagnosis, look at the joints carefully. If
you can find evidence of subchondral
collapse or the typical lucent/sclerotic
appearance of the necrotic bone in the
weight-bearing bone, then
osteonecrosis becomes a much more
likely diagnosis.
3. Patients with sclerotic lesions due to
metastasis often have a history of prior
malignant disease. Ask the patient or
the clinician about this.
4. Likewise patients with sclerotic lesions
due to various drugs or minerals will
tell you what they are taking if you ask
them.
5. When considering congenital causes of
sclerotic lesions, benign causes such as
bone islands or osteopoikilosis usually
have a fairly typical appearance and are
hard to mistake. Osteopetrosis and
pyknodysostosis are likewise hard to
mistake for other entities since the
bones are denser than in any other
disorder, and the long bones tend to
have very tiny medullary canals.
6. When considering trauma as a cause
for sclerotic lesions, remember to check
and see if the areas involved are areas
in the typical distribution for stress
fractures.
7. When considering hyperparathyroidism,
look for evidence of subperiosteal bone
resorption.
8. When considering Paget's disease, it is
extremely helpful to note whether there
is associated bony enlargement. This is
extremely common in Paget's disease
but extremely uncommon with a blastic
metastasis. Another finding classic for
Paget's disease is that it almost always
starts at one end of a bone and then
spreads toward the other end of the
bone
Periosteal Reaction
The periosteum is a membrane several cell
layers thick that covers almost all of every bone.
About the only parts not covered by this
membrane are the parts covered by cartilage.
Besides covering the bone and sharing some of
its blood supply with the bone, it also produces
bone when it is stimulated appropriately. What
does it take to make this happen? Practically
anything that breaks, tears, stretches, inflames,
or even touches the periosteum. So, when some
anonymous process stimulates this reactive
bone formation, eventually we see evidence of it
on some imaging study.
Once we spot this reactive new bone, how do we
deal with it? In the best of all possible worlds,
one would be able to look at the pattern of
periosteal reaction and then give a precise
histological diagnosis. Alas, this is not that kind
of world. We can't give a precise histological
diagnosis. But wait -- it gets worse! We can't
even tell for sure if the underlying process is
benign or malignant! As it turns out, about all
we can do is say with some confidence whether
the process is a benign or an aggressive one.
Why is this? Well, the periosteum is a fairly
promiscuous tissue, and puts on a similar
response to all comers. The main determinant of
how the new bone formation looks is how fast
the abnormal process grows, and has little to do
with any intrinsic properties of the periosteum.
Therefore, any differences in the pattern of
periosteal reaction must arise in the disease
process itself -- not in the periosteum. Again,
evidence of the speed at which these processes
are growing is the main thing we look for when
assessing periosteal reaction. Knowledge of this
speed will help us to differentiate these
processes into two broad categories.
With slow-growing processes, the periosteum
has plenty of time to respond to the process.
That is, it can produce new bone just as fast as
the lesion is growing. Therefore, one would
expect to see solid, uninterrupted periosteal new
bone along the margin of the affected bone.
solid periosteal reaction along the cortex of a
bone
figure after Ragsdale, et al 1981
However, with rapidly growing processes, the
periosteum cannot produce new bone as fast as
the lesion is growing. Therefore, rather than a
solid pattern of new bone formation, we see an
interrupted pattern. This interrupted pattern can
manifest itself in several ways, depending on
just how steadily the lesion grows. If the lesion
grows unevenly in fits and starts, then the
periosteum may have time to lay down a thin
shell of calcified new bone before the lesion
takes off again on its next growth spurt. This
may result in a pattern of one or more
concentric shells of new bone over the lesion.
This pattern is sometimes called lamellated or
"onion-skin" periosteal reaction.

lamellated periosteal reaction
figure after Ragsdale, et al 1981
If the lesion grows rapidly but steadily, the
periosteum will not have enough time to lay
down even a thin shell of bone, and the pattern
may appear quite different. In such cases, the
tiny fibers that connect the periosteum to the
bone (Sharpey's fibers) become stretched out
perpendicular to the bone. When these fibers
ossify, they produce a pattern sometimes called
"sunburst" or "hair-on-end" periosteal reaction,
depending of how much of the bone is involved
by the process.
"sunburst" and "hair-on-end" periosteal reaction
figure after Ragsdale, et al 1981
Osteosarcoma of the distal femur, demonstating
dense tumor bone formation and a sunburst
pattern of periosteal reaction.
Another pattern seen in rapidly growing
processes is called the Codman's triangle. This is
a bit of a misnomer, since there really is not a
complete triangle. When a process is growing
too fast for the periosteum to respond with even
thin shells of new bone, sometimes only the
edges of the raised periosteum will ossify. When
this little bit of ossification is seen tangentially
on a radiograph, it forms a small angle with the
surface of the bone, but not a complete triangle.
So, when a process is growing too fast for even
the Sharpey's fibers to ossify, one may only see
a soft tissue mass arising from the bone,
perhaps with small Codman's triangles at its
margins.
a Codman's triangle
figure after Ragsdale, et al 1981
Soooooo...... what is the significance of all of
these patterns? Well, we can usually
differentiate lesions into one of two categories:
benign vs. aggressive processes. If we see a
solid pattern of periosteal reaction, we can be
fairly confident that we are dealing with a
benign process. How confident? In normal
everyday practice, my estimate is that you can
be about 90 - 95 % confident in this rule(9), but
your mileage may vary. As with many rules in
medicine, there are some caveats associated
with the use of this rule. The main caveat with
this rule is that benign processes and malignant
processes may coexist. The usual way that this
may manifest is when there is a fracture or
infection in the same area as a tumor. In this
case, you may see a fairly complex pattern of
periosteal reaction that demonstrates some
elements that look benign and some that look
very aggressive.
a complex pattern of periosteal reaction
figure after Ragsdale, et al 1981
The take home point here is that complex • hypertrophic pulmonary
patterns like this may be very misleading, and osteoarthropathy
should be interpreted with caution. In general,
though, the more aggressive the pattern of
• deep venous thrombosis (lower
periosteal reaction, the greater the chance that extremity)
you are dealing with a malignancy. Causes of Aggressive Periosteal Reaction
Here are partial lists of causes of both solid and • osteomyelitis
aggressive periosteal reaction: • malignant neoplasms
Causes of Solid Periosteal Reaction o osteosarcoma
• infection o chondrosarcoma
• benign neoplasms o fibrosarcoma
o osteoid osteoma o lymphoma
• eosinophilic granuloma o leukemia
o metastasis

http://www.rad.washington.edu/academics/academic-sections/msk/teaching-
materials/online-musculoskeletal-radiology-book/axial-arthritis

rad.washington.edu/academics/academic-sections/msk/.../axial-arthritis