AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• Mri
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• Mri
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

Background

Calcium pyrophosphate deposition disease (CPDD) is a variety of arthritis caused by the deposition of calcium pyrophosphate crystals. CPDD is divided into several varieties, primarily pseudogout and chondrocalcinosis. Synovial calcium pyrophosphate crystals, seen on polarizing microscopy, characterize pseudogout, an acute goutlike arthritis.

Chondrocalcinosis is recognized as calcification within fibrous or hyaline cartilage structures. Radiologically, a dense line within the hyaline cartilage parallels the articular surface, often resulting in a calcified hyaline cartilage surface. This can be recognized grossly as a calcified sheet reflecting over the articular surface and as concretions of calcium pyrophosphate exuded beyond the subchondral articular surface. Pseudogout and chondrocalcinosis may overlap with each other and with other varieties.

Other varieties appear ill defined and include a subgroup referred to as pseudorheumatoid. Periarticular metacarpal phalangeal and interphalangeal joint calcification may be a component of that form of CPDD. Radiocarpal articular surface indentation (an unusual joint to be affected in osteoarthritis [OA]) is also considered evidence of CPDD, as are large subchondral cysts (ie, geodes), which rarely occur.

Pseudorheumatoid CPDD has a polyarticular character. One variety of idiopathic CPDD with destructive peripheral arthritis has been reported. Bony fragmentation or a crumbling appearance, which may simulate a neuropathic joint, characterizes this variety.

Pathophysiology

CPDD is the result of an inflammatory cascade response to the deposition of calcium pyrophosphate crystals. Enzyme or saturation abnormalities allow the formation of excess pyrophosphate, which salts out, especially in hyaline and fibrous cartilage. Individuals with CPDD may have more than one type of crystal present (eg, hydroxyapatite in addition to pyrophosphate).

A chromosome t(2;10) addition has been described in one case involving the temporomandibular joint.

Frequency

United States

Primary CPDD is a disease of aging, affecting approximately 5% of the population aged 28-96 years.

International

The incidence appears to be the same as in the United States.

Mortality/Morbidity

Morbidity is related to joint pain and disability caused by arthritis. CPDD may be asymptomatic, with episodes of hyperacute arthritis (termed pseudogout), or may be a chronic arthritis.

Sex

The male-to-female ratio is equal.

Age

Primary CPDD is a disease of aging, affecting approximately 5% of the population aged 28-96 years. CPDD is rare until age 30 years, then increases exponentially until age 75 years, when it plateaus.

Anatomy

CPDD typically affects hyaline and fibrous cartilage.

Clinical Details

CPDD can be divided into primary and secondary varieties. Secondary refers to CPDD associated with rheumatoid arthritis or spondyloarthropathy.

Table 1. Distribution Pattern (%) of Nonerosive Component of Primary CPDD in Skeletal and Clinical Populations

The distribution of CPDD in individuals with secondary CPDD (eg, rheumatoid arthritis, spondyloarthropathy) is identical to that noted in those with primary CPDD.

Primary CPDD can also be divided into familial, metabolic, and idiopathic varieties. The pattern of joint involvement differs among the varieties.

The familial variety of CPDD tends to occur earlier in life than the idiopathic variety. Metabolic causes and associations with CPDD include hypothyroidism, hyperparathyroidism, hypophosphatasia, hypomagnesemia, gout, ochronosis, Wilson disease, acromegaly, and Paget disease.

Table 2. Joint Distribution Pattern (%) of CPDD in Familial, Idiopathic, and Metabolic (eg, hemochromatosis [hemo] and ochronosis [ochro]) Varieties

Hemochromatosis is a disorder of iron metabolism in which iron accumulates in and damages body tissues, including joints.

Wilson disease consists of abnormal metabolic accumulation, specifically of copper.

Ochronosis is another storage disease in which homogentisic acid accumulates as a result of a deficiency of the metabolizing enzyme.

While the metabolic varieties of CPDD are usually inherited (ie, genetic), an acquired form of hemochromatosis (analogous to hydroquinone-induced ochronosis) reportedly occurs, either from ingesting excess amounts of iron or secondary to excess iron release in hemolytic anemia.

Additional clinical signs include confusion, fever, and meningismus.

Preferred Examination

Routine radiographs usually reveal the pathology. Aspiration of joint fluid may be necessary to identify the type of crystals.

CT scanning is occasionally used.

MRI is rarely used.

Limitations of Techniques

MRI does not visualize calcific structures well.

DIFFERENTIALS

Section 3 of 11  

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• Introduction
• Differentials
• Radiograph
• CT SCAN
• Mri
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

Other Problems to be Considered

Basic calcium phosphate crystal deposition
Calcinosis
Calcium oxalate arthritis
Chondrosarcoma
Erosive OA
Hydroxyapatite arthritis
Joint replacement failure
Juxtacortical chondroma
Neoplasm
Osteonecrosis
Prosthetic joint breakdown
Secondary OA
Spondyloarthropathy
Tumoral calcinosis

RADIOGRAPH

Section 4 of 11  

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• Radiograph
• CT SCAN
• Mri
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

Findings

Chondrocalcinosis is recognized by calcification within fibrous or hyaline cartilage structures (see Image 1, Image 6), which appears on radiographs as a dense line within the hyaline cartilage that parallels the articular surface. Grossly, this is recognized as a calcified sheet reflecting over the articular surface and as white, hard, 3- to 4-mm concretions of calcium pyrophosphate or hydroxyapatite exuded beyond the subchondral articular surface. A third variety presents with periarticular metacarpal phalangeal and interphalangeal joint calcification.

Just as the calcium pyrophosphate deposition disease (CPDD) pattern can mimic rheumatoid arthritis, it can also mimic OA. While the radiocarpal and metacarpal phalangeal joints are usually not affected in OA, OA-like changes in these locations are highly suggestive of CPDD. Large subchondral cysts (ie, geodes; see Image 2) are also rarely noted in CPDD. The pseudorheumatoid variety of CPDD is an erosive disease. Another variety of CPDD is described as a destructive peripheral arthritis associated with bony fragmentation.

CPDD is strongly suggested when findings indicative of degenerative OA are observed in unusual locations, such as in the shoulder and elbow, which are nonweightbearing joints that seldom manifest degenerative OA.

Indentation of the radiocarpal joint and joint space narrowing with sclerosis are indicators of CPDD (see Image 7). Tendon calcification and fluffy calcification of soft tissue within joints or bursae may also occur. The latter, termed a tophus, is analogous to that occasionally found in gout.

Involvement of the spine in CPDD manifests as calcification of the nucleus pulposus or anulus fibrosus (see Image 4). The zygapophyseal and costovertebral joints are spared.

Disruption of cortical margins (ie, erosion) is present in approximately one eighth of patients with CPDD, usually as an isolated phenomenon (see Image 5). Articular surface localization of erosion is site dependent. While metacarpal phalangeal, proximal interphalangeal, and distal interphalangeal erosions tend to occur subchondrally, involvement of other joints tends to be marginal (eg, bare area) in distribution. Subchondral erosions are not sharply defined; rather, they have a smudged appearance (see Image 3).

The nonerosive component of CPDD is symmetric in two thirds of patients, although typically pauciarticular (80%). CPDD predominantly affects knee, shoulder, wrist, and metacarpal phalangeal joints in patterns reproducible across multiple populations.

The density of bone in the vicinity of joints is unchanged. Radiologic examination confirms the presence of calcific shelves and concretions. Also noted are sharply defined cysts that communicate with the articular surface. The cysts have characteristic sclerotic margins. Demonstrated communication of such lesions with the articular surfaces emphasizes that CPDD may have an erosive component.

Erosions of the pseudorheumatoid variety of CPDD (ie, 5% of patients with CPDD) are essentially limited to the small joints of the hands and feet (see Image 3).

Table 3. Distribution Pattern (%) of Erosions in Patients With Primary CPDD

The crumbling lesions of pseudorheumatoid CPDD differ from those of other varieties, which are predominantly marginal in location and affect only 1-2 joints. The joints affected (predominantly shoulder, metacarpal phalangeal, proximal interphalangeal, distal interphalangeal) mirror those of the nonerosive component of CPDD. While the lesions tend to be subchondral in distribution and without new bone formation, 8 joints are typically affected. However, the extent of nonerosive CPDD manifestations is more extensive than that observed in individuals with other CPDD patterns.

Degree of Confidence

Chondrocalcinosis is pathognomonic for the CPDD category. Some divide this into calcium pyrophosphate and hydroxyapatite varieties; however, since the crystals often co-occur, the term CPDD may be reasonable. Crumbling erosions and radiocarpal joint indentation are pathognomonic for CPDD.

CPDD is strongly suggested when findings indicative of degenerative OA are observed in unusual locations, such as in the shoulder and elbow, which are nonweightbearing joints that seldom manifest degenerative OA. Isolated involvement of the patellofemoral joint is also suggestive.

False Positives/Negatives

Radiologic findings may be within reference range in a patient with crystals documented with a polarizing microscopic examination of the joint fluid.

The breakdown of joint prostheses may produce a radiodense linear pattern that mimics CPDD.

CT SCAN

Section 5 of 11  

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• Introduction
• Differentials
• Radiograph
• CT SCAN
• Mri
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

Findings

The pattern on CT scans may show a calcific mass with lobulated configuration, typically in the ligamentum flavum or within the joint capsule. Septumlike low-density areas are noted within the mass. Pressure erosions may be noted with disruption of adjacent bony cortex. Fine granular calcifications may also be noted. Subchondral cysts or erosions, as well as fractures (eg, odontoid), may be observed.

Degree of Confidence

Routine radiographs usually reveal calcium pyrophosphate deposition disease (CPDD) more accurately.

False Positives/Negatives

The breakdown of prosthetic joints may produce linear patterns of radiodensity, mimicking CPDD.

MRI

Section 6 of 11  

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• Introduction
• Differentials
• Radiograph
• CT SCAN
• Mri
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

Findings

MRI has low sensitivity for detecting calcification but can display massive deposition. Calcifications of chondrocalcinosis present on MRI as signal void or decreased signal intensity, although increased T1-weighted signal intensity is rarely noted.

T1-weighted images reveal low-signal intensity with punctate signal void. T2-weighted images vary in signal intensity, dependent on crystal concentration and the amount of associated granulation tissue and fibrosis. Rim enhancement is rarely noted. Gadolinium-enhanced images demonstrate peripheral enhancement. An associated fracture produces lines of low signal intensity on both T1-weighted and T2-weighted spin echo, with marrow edema.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. As of late December 2006, the FDA had received reports of 90 such cases. Worldwide, over 200 cases have been reported, according to the FDA. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble

movingor straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Degree of Confidence

Since MRI does not visualize calcific structures well, CT or radiographic confirmation is required.

False Positives/Negatives

The breakdown of prosthetic joints may produce signal deficits that suggest calcific deposits. Additionally, MRI findings may mimic a meniscal tear.

ULTRASOUND

Section 7 of 11  

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• Introduction
• Differentials
• Radiograph
• CT SCAN
• Mri
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

Findings

Synovitis and calcific deposits may be noted on ultrasound. A hypoechoic area may be found in the cartilage.

In anecdotal reports in the literature, amplitude Doppler or power Doppler ultrasound has been used to evaluate the synovial hyperemia associated with inflammation in calcium pyrophosphate deposition disease (CPDD) arthropathy in the hands. The degree of abnormal blood flow on Doppler appears to be in proportion to the severity of the clinical manifestations.

Degree of Confidence

Ultrasound lacks specificity.

NUCLEAR MEDICINE

Section 8 of 11  

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• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

Findings

Uptake of bone-seeking radiopharmaceuticals (such as technetium Tc 99m–labelled diphosphonate) is prominent in affected joints. Extraosseous calcific deposits may also take up the radioisotope.

Degree of Confidence

Nuclear imaging procedures are highly sensitive; however, they lack specificity in this setting.

False Positives/Negatives

Any cause of localized tissue hyperemia results in increased deposition of radiotracer within the bone and joints. Recent joint trauma or surgery or any type of arthritis may produce essentially identical results.

INTERVENTION

Section 9 of 11  

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• Introduction
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• Radiograph
• CT SCAN
• Mri
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

No radiographic intervention is indicated. Calcium pyrophosphate deposition disease (CPDD) is treated medically or surgically. Occasionally, ultrasound guidance may be provided to assist with arthrocentesis, but this is usually not necessary.

Medical/Legal Pitfalls

• Failure to differentiate CPDD from rheumatoid arthritis may expose the patient to the potential toxicity of cytotoxic drugs (eg, methotrexate) with no proven efficacy in treating CPDD

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• Mri
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

Media file 1:  Anteroposterior radiograph of knee. Radiodense lines paralleling the articular surface and calcification in the menisci of the knee identify the presence of chondrocalcinosis.
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Media file 2:  Anteroposterior radiograph of navicular cyst. These cysts are not specific for calcium pyrophosphate deposition disease. May be posttraumatic or ganglion cysts.
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Media type:  X-RAY

Media file 3:  Magnified image demonstrating chondrocalcinosis within the meniscal cartilage of the knee.
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Media type:  X-RAY

Media file 4:  Crumbling-type erosions of calcium pyrophosphate deposition disease in the metacarpal phalangeal and proximal and distal interphalangeal joints. A. Dorsal view of metacarpal phalangeal joints with a smudged appearance. B. Anteroposterior radiograph of metacarpal phalangeal joints. Ill-defined loss of articular surface is associated with general preservation of perilesional bone density. C. Ventral view of proximal phalanges with a smudged appearance. D. Anteroposterior radiograph of the hand. An ill-defined loss of articular surface is associated with general preservation of perilesional bone density.
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Media type:  X-RAY

Media file 5:  Spine involvement in calcium pyrophosphate deposition disease. A. Anterior view of lumbar spine. Apparent bridging is not associated with erosions at the anterior superior and anterior inferior borders of the vertebral bodies (in contrast to that seen in spondyloarthropathy). B. Lateral radiograph of lumbar spine with calcification of vertebral disks.
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Media type:  X-RAY

Media file 6:  Sharply defined region of decreased bone density (ie, cyst) with sclerotic margins, which on rotation is seen to communicate with the articular surface. A. Anteroposterior radiograph of proximal humerus. B. Oblique radiograph of proximal humerus.
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Media type:  X-RAY

Media file 7:  Posteroanterior radiograph of the wrist. Note the chondrocalcinosis of the triangular fibrocartilage (TFCC) and indentation of the radiocarpal joint.
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Media type:  X-RAY

Media file 8:  Calcium pyrophosphate deposition disease of the wrist. Again note calcification within the substance of the triangular fibrocartilage and evidence of laxity or disruption of the scapholunate ligament, with widening of the scapholunate interval (occasionally known as the Terry Thomas or David Letterman sign).
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Media type:  X-RAY

Media file 9:  Oblique view of the surface of the distal radius. Note indentation of radiocarpal joint.
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Media type:  X-RAY

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• Mri
• Ultrasound
• Nuclear Medicine
• Intervention
• Multimedia
• References

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Article Last Updated: Apr 3, 2007