Arthritis

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.

bridging osteophytes in the spine of a patient with degenerative disk disease Syndesmophytes Syndesmophytes are generally seen only in the seronegative spondyloarthropathies. These are due to inflammation and ossification of the outer fibers of the annulus fibrosus, known as the Sharpey's fibers. This is classically seen in ankylosing spondylitis. In the other seronegative spondyloarthropathies, one usually sees paravertebral ossification which forms in the paravertebral connective tissue at some distance from the spine. In practice, it may be very difficult to distinguish osteophytes from syndesmophytes or paravertebral ossification.

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. Erosions In general, the presence of erosions bespeaks some type of inflammatory disease, whether the erosions are due to synovial hypertrophy, crystalline deposits, or infection. Crystal deposition In general, this is indicative of one of the crystalline arthropathies -- either CPPD or hydroxyapatite. Sclerosis Not an especially specific finding in spinal arthropathy. Ankylosis This may occur as a result of many degenerative 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.

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 spondylitis

SI and facet joints must be normal

Degenerative nuclear disease

Disc spaces must be of normal height

Ossification must be seen along four contiguous 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 Degenerative annular disease

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

arthroplasty, in an attempt to prevent or diminish the development of heterotopic bone formation after surgery.

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.

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

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 T2weighted 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 Group

Young (< 20 years)

Age of Onset

Disorder

Juvenile chronic arthritis < 20 years Septic arthritis

Ankylosing spondylitis Reiter's

onset 15 35 years

Middle (> 20 years)

Enteropathic arthropathies

Young adults

Rheumatoid arthritis Psoriatic arthritis

25 - 55 years

Older patients (> 55 years)

> 55 years

Osteoarthritis DISH CPPD

Arthropathies with Male Predominance Disorder

male:female ratio

Ankylosing spondylitis

4:1 to 10:1

Psoriatic

2:1 to 3:1, but controversial

Reiter's

5:1 to 50:1

Gout

20:1

DISH

3:2

CPPD

1:1

disorders. Even though over 90 different rheumatic diseases are recognized by the American College of Rheumatology, only three entities are commonly seen in most clinical radiology practices, even including those located in large tertiary medical centers. Osteoarthritis (a.k.a. degenerative joint disease) is the most commonly seen form of appendicular arthritis. The other two commonly seen arthropathies are rheumatoid arthritis and calcium pyrophosphate dihydrate (CPPD) deposition disease. Less common arthropathies that may manifest radiographic findings in the appendicular skeleton include septic arthritis, and gout. Most other appendicular arthropathies are seen only rarely. 2. Radiographic Hallmarks In George Orwell's Animal Farm, it is stated that "All animals are equal. But some animals are more equal than others." This principle is manifested in the appendicular arthropathies, where some radiographic findings are quite specific and can quickly lead one to the correct diagnosis. Other findings are less specific and are usually unhelpful in ordering one's differential diagnosis. In a diarthrodial joint, osteophytes are the sine qua non of osteoarthritis. Osteophytes can be seen in both primary and secondary 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

Primary osteoarthritis (> 45 years) CPPD

marked osteophytosis (arrows) is seen in the DIP and PIP joints in these fingers

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. Appendicular Arthritis 1. Sutton's Law This law has been ascribed to Willie Sutton, a famous bank robber. When asked why he robbed banks, he reportedly said, "Because that's where the money is." In the radiographic evaluation of appendicular arthropathies, the "money" is generally in a relatively small handful of

osteophytosis (arrow) is noted at the articular margin of the femoral head Osteophytes can also be seen at various entheses (sites of tendinous or ligamentous attachment to bone), often due to altered or increased stress there. In general, the presence of erosions bespeaks some type of inflammatory disease, whether the

erosions are due to synovial hypertrophy, crystalline deposits, or infection. In rheumatoid arthritis, 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 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 erosions (arrows) are noted in the periarticular areas of the toes in this patient with rheumatoid arthritis

chondrocalcinosis is seen in the triangular fibrocartilage of this wrist

multiple erosions and marked joint space narrowing are noted in a pancarpal distribution in this patient with rheumatoid arthritis

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.

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 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 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 hands

joint compartments of the wrist -- CMC (first carpometacarpal), CCMC (common carpometacarpal), ST (scaphotrapezial), MC (midcarpal), RC (radiocarpal), and DRUJ (distal radioulnar joint)

typical distribution of arthritis in the wrists

typical distribution of arthritis in the 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 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 (years)

TUMOR

1

neuroblastoma

1 - 10

Ewing's of tubular bones

10 - 30

osteosarcoma, Ewing's of flat bones

30 - 40

reticulum cell sarcoma (Primary histiocytic lymphoma), fibrosarcoma, parosteal osteosarcoma, malignant giant cell tumor, lymphoma

40 +

metastatic carcinoma, multiple myeloma, chondrosarcoma

Size 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 anything, it tends to greatly underestimate the extent of the lesion. However, it provides a convenient first-order approximation of the extent (a lower bound on its size) while the early workup is being arranged. Definitive assessment of the pretreatment extent of a lesion will require MR or CT. 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 stimuli, and generally responds to one of the processes in FOGMACHINES by either removing bone or creating bone. That's right! The bone itself does the removing or creating of bone not the disorder involving the bone. At the AFIP, they are fond of saying that the only things that can remove bone are osteoclasts and orthopedic surgeons. I agree with this rule, but would also add talented amateurs to the list (lawnmower and saw accidents, auto crashes, blast injuries, 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 laying down new bone around the margins of the lesion. This generally has the effect of

producing a sclerotic and usually distinct margin around the lesion. If process grows more rapidly, the bone may only have time to retreat before the lesion, and not have time to lay down this sclerotic rim. Solitary lucent lesions in bone with a distinct margin are generally called "geographic" lesions, whether or not they have a sclerotic rim.

geographic lesion with geographic lesion with ill-defined rim well-defined rim If the lesion grows more rapidly still, there may not be time for the bone to retreat in an orderly manner, and the margin may become ill-defined. Rather than a single discrete lesion, we may see several ill-defined foci of lucency. This has been termed a "moth-eaten" pattern.

a "moth-eaten" lesion If, alas, the process grows more rapidly still, then the bone's retreat may become disorderly indeed. Continuing this battlefield analogy, the boundary between normal and abnormal bone may be lost altogether, with only a very illdefined pattern of lucency seen, caused by many small, irregular holes in the bone, left behind by osteoclasts. This is an extremely aggressive pattern, sometimes called a "permeative" pattern.

permeative pattern

normal bone

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

3. 4.

5.

6.

think of one of these three entities, also think of the other two. Giant cell tumors nearly always occur near a joint surface. 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. Lucent lesions of the sternum should be considered malignant until proven otherwise (Helms CA, personal communication, 1983).

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 o

hemangiomas infarct

•

Infection

•

Neoplasm o primary

o

o

•

• • •

 

osteoma

  

prostate

osteosarcoma metastatic breast other

Congenital o bone islands o osteopoikilosis o osteopetrosis o pyknodysostosis Autoimmune

o

fracture (stress)

•

Infection

•

Neoplasm o primary

o

o

•

Neoplasm o metastatic

  

•

prostate breast other

Drugs

o o

Vitamin D fluoride

Congenital o osteopetrosis o pyknodysostosis

Endocrine/Metabolic o hyperparathyroidism You may have been surprised to see metastatic disease listed as a leading cause for diffuse sclerotic bones. It is true that the usual appearance of skeletal metastases is that of focal lesions -- diffuse sclerosis occurs in only a small fraction of cases of skeletal metastases. However, cancers that metastasize to bone are very common. The lesson here is that when we are dealing with a very common disorder, even its less common presentations will be seen commonly.

chronic osteomyelitis

 

osteoma

  

prostate

osteosarcoma metastatic breast other

Congenital o bone islands o osteopoikilosis Trauma

•

•

Trauma

Endocrine/Metabolic o hyperparathyroidism o Paget's disease One of the first things you should notice about sclerotic bone lesions is whether they are single and focal, multifocal, or diffuse. You can then customize the above differential for whichever pattern of sclerosis that you see. Generally, this just follows common sense -- some lesions should logically be expected to be focal, others multifocal, and yet others diffuse or systemic. For example: Differential Diagnosis of Focal or Multifocal Sclerotic Bone Lesions • Vascular o hemangiomas o infarct

•

•

Vitamin D fluoride

Inflammatory/Idiopathic

fracture (stress)

Endocrine/Metabolic o Paget's disease As you can see, by just dropping the items that tend to cause generalized sclerosis, we have generated a fairly good differential for focal lesions. The differential for multifocal lesions happens to be identical to that for focal lesions. Differential Diagnosis of Diffuse Sclerotic Bone Lesions • Vascular o infarct (e.g. sickle cell)

Drugs

o o • •

chronic osteomyelitis

o •

diffuse sclerotic metastases to the pelvis, sacrum and femurs Wise Sayings About Sclerotic Lesions There are a number of other helpful findings you can look for that can help you to cone in on or away from specific entities in one of these differential lists. 1. Most cases of chronic osteomyelitis look pretty nonspecific. However, if one sees sinus tracts associated with a sclerotic area, one should strongly consider osteomyelitis. 2. Diffuse skeletal infarcts can be a 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.

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.

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

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 patterns like this may be very misleading, and should be interpreted with caution. In general, though, the more aggressive the pattern of periosteal reaction, the greater the chance that you are dealing with a malignancy. Here are partial lists of causes of both solid and aggressive periosteal reaction: Causes of Solid Periosteal Reaction • infection

• •

benign neoplasms o osteoid osteoma eosinophilic granuloma

•

hypertrophic pulmonary osteoarthropathy • deep venous thrombosis (lower extremity) Causes of Aggressive Periosteal Reaction • osteomyelitis

•

malignant neoplasms o osteosarcoma o chondrosarcoma o fibrosarcoma o lymphoma o leukemia o metastasis

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