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Imaging in Calcium Pyrophosphate Deposition Disease

  • Author: Bruce M Rothschild, MD; Chief Editor: Felix S Chew, MD, MBA, MEd  more...
 
Updated: Jan 11, 2016
 

Overview

Calcium pyrophosphate deposition disease (CPDD) is a type of arthritis caused by the deposition of calcium pyrophosphate crystals.

Clinical Image Atlas: View clinical images on the features, causes, epidemiology, diagnosis, and treatment of Gout.

Primary calcium pyrophosphate deposition disease

Calcium pyrophosphate deposition disease (CPDD) is divided into several varieties, primarily pseudogout and chondrocalcinosis. Synovial calcium pyrophosphate crystals, seen on polarizing microscopy, characterize pseudogout, an acute goutlike arthritis.[1, 2]

Phosphate-to-pyrophosphate ratios less than 3 result in CPPD formation. When the ratio is greater than 100, hydroxyapatite crystals form.[3] This ratio is controlled by a balance between ank/ANKH, interference with ectonucleotide pyrophosphatase/phosdiesterase activity, a protein referred to as PiT-1, and tissue-nonspecific alkaline phosphatase. Formation of CPPD crystals requires levels of pyrophosphate 10-40 times normal serum levels.

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 (see the images below). 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.[4]

Anteroposterior radiograph of knee. Radiodense lin Anteroposterior radiograph of knee. Radiodense lines paralleling the articular surface and calcification in the menisci of the knee identify the presence of chondrocalcinosis.
Magnified anteroposterior radiograph of knee demon Magnified anteroposterior radiograph of knee demonstrating chondrocalcinosis within the meniscal cartilage of the knee.

Other varieties appear ill defined and include a subgroup referred to as pseudorheumatoid. Periarticular metacarpophalangeal and interphalangeal joint calcification may be a component of that form of calcium pyrophosphate deposition disease (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 (see the images below).

Anteroposterior radiograph of navicular cysts. The Anteroposterior radiograph of navicular cysts. These cysts are not specific for calcium pyrophosphate deposition disease. They may be posttraumatic or ganglion cysts.
Oblique view of the surface of the distal radius. Oblique view of the surface of the distal radius. Note the indentation of the radiocarpal joint.

Pseudorheumatoid calcium pyrophosphate deposition disease (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 (see the following image).

Crumbling-type erosions of calcium pyrophosphate d Crumbling-type erosions of calcium pyrophosphate deposition disease in the metacarpophalangeal and proximal and distal interphalangeal joints. A: Dorsal view of metacarpophalangeal joints with a smudged appearance. B: Anteroposterior radiograph of metacarpophalangeal 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.

The skeletal and clinical distribution pattern of nonerosive components of primary calcium pyrophosphate deposition disease (CPDD) are shown in the table below.

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

Joint Skeletal, % Clinical, %
Knee 54 41-99
Shoulder 38 16-50
Radiocarpal 35 6-43
Metacarpophalangeal 30 19-50
Elbow 24 23-33
Proximal interphalangeal 21 19
Distal interphalangeal 18 19
Hip 16 18-27
Metatarsophalangeal 13 2
Ankle 10 7-11
Interphalangeal 4 2

 

Secondary calcium pyrophosphate deposition disease

The variety of calcium pyrophosphate deposition disease (CPDD) is associated with rheumatoid arthritis or spondyloarthropathy. The distribution of CPDD in individuals with secondary CPDD (eg, rheumatoid arthritis, spondyloarthropathy) is identical to that noted in those with primary CPDD and is shown in the table below. Craniometaphyseal dysplasia is related to ANKH (a transmembrane protein) mutations.[3]

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

Joint Familial, %  



Idiopathic, %



Metabolic



Hemo, %



 



Metabolic



Ochro, %



Knee 62 41-99 89 63-99
Radiocarpal 24 6-43 100 3-29
Shoulder 19 16-50 0 49-86
Elbow 14 23-33 11 9-29
Hip 10 18-27 0 43-57
Metatarsophalangeal 8-10 2 0 0
Metacarpophalangeal 5-14 40-50 44 29
Ankle 0-15 7-11 33 0
Spine 0-15 1-17 0-15 100

 

Differentials and other problems to be considered

The differential diagnosis includes ankylosing spondylitis, diffuse idiopathic skeletal hyperostosis, Gout, meniscal tears, neuropathic arthropathy (Charcot joint), Osgood-Schlatter disease, primary osteoarthritis, osteochondritis dissecans, osteochondroma and osteochondromatosis, classic and variant osteosarcomas, rheumatoid arthritis of the hands and spine, septic arthritis, spinal stenosis, and synovial osteochondromatosis.

Other conditions that should be considered are basic calcium phosphate crystal deposition, calcinosis, calcium oxalate arthritis, chondrosarcoma, erosive osteoarthritis, hydroxyapatite arthritis, joint replacement failure, juxtacortical chondroma, neoplasm, osteonecrosis, prosthetic joint breakdown, secondary osteoarthritis, spondyloarthropathy, and tumoral calcinosis.

Radiologic intervention

No radiographic intervention is indicated. Occasionally, ultrasonographic guidance may be provided to assist with arthrocentesis, but this is usually not necessary.

Special concerns

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.

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Radiography

Routine radiographs usually reveal the pathology of calcium pyrophosphate deposition disease (CPDD). Recent recommendations from the European League Against Rheumatism suggest that radiographic chondrocalcinosis supports the diagnosis of CPPD, but its absence does not exclude it.[5] Chondrocalcinosis is recognized by calcification within fibrous or hyaline cartilage structures (as shown in the images below), 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 metacarpophalangeal and interphalangeal joint calcification.

Anteroposterior radiograph of knee. Radiodense lin Anteroposterior radiograph of knee. Radiodense lines paralleling the articular surface and calcification in the menisci of the knee identify the presence of chondrocalcinosis.
Magnified anteroposterior radiograph of knee demon Magnified anteroposterior radiograph of knee demonstrating chondrocalcinosis within the meniscal cartilage of the knee.
Sharply defined region of decreased bone density ( 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.

Just as the calcium pyrophosphate deposition disease (CPDD) pattern can mimic rheumatoid arthritis, it can also mimic osteoarthritis. Whereas the radiocarpal and metacarpophalangeal joints are usually not affected in osteoarthritis, osteoarthritislike changes in these locations are highly suggestive of CPDD (as shown in the images below).

Calcium pyrophosphate deposition disease of the wr Calcium pyrophosphate deposition disease of the wrist. Again, note calcification within the substance of the triangular fibrocartilage (TFCC) 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).
Oblique view of the surface of the distal radius. Oblique view of the surface of the distal radius. Note the indentation of the radiocarpal joint.

Large subchondral cysts (ie, geodes; see the image below) are also rarely noted in calcium pyrophosphate deposition disease (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.

Anteroposterior radiograph of navicular cysts. The Anteroposterior radiograph of navicular cysts. These cysts are not specific for calcium pyrophosphate deposition disease. They may be posttraumatic or ganglion cysts.

Calcium pyrophosphate deposition disease (CPDD) is strongly suggested when findings indicative of degenerative osteoarthritis are observed in unusual locations, such as in the shoulder and elbow, which are non–weight-bearing joints that seldom manifest degenerative osteoarthritis.

Indentation of the radiocarpal joint and joint space narrowing with sclerosis are indicators of calcium pyrophosphate deposition disease (CPDD) (see the image below). 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.

Posteroanterior radiograph of the wrist. Note the Posteroanterior radiograph of the wrist. Note the chondrocalcinosis of the triangular fibrocartilage (TFCC) and indentation of the radiocarpal joint.

Involvement of the spine in calcium pyrophosphate deposition disease (CPDD) manifests as calcification of the nucleus pulposus or anulus fibrosus (see the image below). The zygapophyseal and costovertebral joints are spared.

Spine involvement in calcium pyrophosphate deposit Spine involvement in calcium pyrophosphate deposition disease. A: Anterior view of lumbar spine. Apparent bridging is not associated with erosions at the anterosuperior and anteroinferior borders of the vertebral bodies (in contrast to that seen in spondyloarthropathy). B: Lateral radiograph of lumbar spine with calcification of vertebral disks.

Disruption of cortical margins (ie, erosion) is present in approximately one eighth of patients with calcium pyrophosphate deposition disease (CPDD) , usually as an isolated phenomenon (see the image below).

Sharply defined region of decreased bone density ( 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.

Articular surface localization of erosion is site dependent. Although metacarpophalangeal, 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 the images below).

Anteroposterior radiograph of knee. Radiodense lin Anteroposterior radiograph of knee. Radiodense lines paralleling the articular surface and calcification in the menisci of the knee identify the presence of chondrocalcinosis.
Magnified anteroposterior radiograph of knee demon Magnified anteroposterior radiograph of knee demonstrating chondrocalcinosis within the meniscal cartilage of the knee.

The nonerosive component of calcium pyrophosphate deposition disease (CPDD) is symmetric in two thirds of patients, although typically pauciarticular (80%). CPDD predominantly affects knee, shoulder, wrist, and metacarpophalangeal 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 calcium pyrophosphate deposition disease (CPDD) may have an erosive component.

Erosions of the pseudorheumatoid variety of calcium pyrophosphate deposition disease (CPDD) (ie, 5% of patients with CPDD) are essentially limited to the small joints of the hands and feet (see the image below).[6]

Crumbling-type erosions of calcium pyrophosphate d Crumbling-type erosions of calcium pyrophosphate deposition disease in the metacarpophalangeal and proximal and distal interphalangeal joints. A: Dorsal view of metacarpophalangeal joints with a smudged appearance. B: Anteroposterior radiograph of metacarpophalangeal 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.

The table below delineates the distribution pattern of erosions in calcium pyrophosphate deposition disease (CPDD).

Table 3. Distribution Pattern (%) of Erosions in Patients With Primary CPDD (Open Table in a new window)

Joint Erosions, %
Proximal interphalangeal 12
Metacarpophalangeal 10
Distal interphalangeal 10
Shoulder 9
Metatarsophalangeal 6
Radiocarpal 2
Knee 2
Interphalangeal 2
Elbow 1
Ankle 1
Hip 0

 

The crumbling lesions of pseudorheumatoid calcium pyrophosphate deposition disease (CPDD) differ from those of other varieties, which are predominantly marginal in location and affect only 1-2 joints (see the image below).

Crumbling-type erosions of calcium pyrophosphate d Crumbling-type erosions of calcium pyrophosphate deposition disease in the metacarpophalangeal and proximal and distal interphalangeal joints. A: Dorsal view of metacarpophalangeal joints with a smudged appearance. B: Anteroposterior radiograph of metacarpophalangeal 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.

The joints affected (predominantly shoulder, metacarpophalangeal, proximal interphalangeal, distal interphalangeal) mirror those of the nonerosive component of calcium pyrophosphate deposition disease (CPDD). Although 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.

What has been previously called erosive osteoarthritis appears to be part of the spectrum of CPPD. The crumbling erosions are characteristic.[7]

Imaging pearls

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

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

Calcium pyrophosphate deposition disease (CPDD) is strongly suggested when findings indicative of degenerative osteoarthritis are observed in unusual locations, such as in the shoulder and elbow, which are non–weight-bearing joints that seldom manifest degenerative osteoarthritis. Isolated involvement of the patellofemoral joint is also suggestive.

The breakdown of joint prostheses may produce a radiodense linear pattern that mimics calcium pyrophosphate deposition disease (CPDD).

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Computed Tomography

The pattern of calcium pyrophosphate deposition disease (CPDD) on CT scans may show a calcific mass with a lobulated configuration, typically in the ligamentum flavum or within the joint capsule. Within the mass are septumlike low-density areas. In addition, 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.[8]

Routine radiographs usually reveal calcium pyrophosphate deposition disease (CPDD) more accurately. Also, the breakdown of prosthetic joints may produce linear patterns of radiodensity, mimicking CPDD.

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Magnetic Resonance Imaging

Calcifications of chondrocalcinosis present on MRI as a signal void or decreased signal intensity, although increased T1-weighted signal intensity is rarely noted.[9, 10] High-field MRI is especially effective for visualization of CPPD deposits.[11]

T1-weighted images reveal low-signal intensity with punctate signal void. T2-weighted images vary in signal intensity, depending 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 have been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Systemic Fibrosis. 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. 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 moving or 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.

MRI has low sensitivity for detecting calcification but can display massive deposition. Because MRI does not visualize calcific structures well, CT scanning or radiographic confirmation is required. In addition, the breakdown of prosthetic joints may produce signal deficits that suggest calcific deposits. MRI findings may also mimic a meniscal tear.

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Ultrasonography

Synovitis and calcific deposits may be noted on ultrasonography. A hypoechoic area may be found in the cartilage.[12, 13, 14, 15, 16, 8]

The European League Against Rheumatism’s systematic review of research evidence suggests that ultrasonography of the knee is sensitive and specific for detecting CPDD crystals, and may be more effective than conventional x-rays.[5]

Ultrasound joint surveys reveal that CPPD involves at least 2 sites (mean = 4 sites).[17]

In anecdotal reports in the literature, amplitude Doppler or power Doppler ultrasonography 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 ultrasonograms appears to be in proportion to the severity of the clinical manifestations.

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Nuclear Imaging

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

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

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Contributor Information and Disclosures
Author

Bruce M Rothschild, MD Professor of Medicine, Northeast Ohio Medical University; Adjunct Professor, Department of Biomedical Engineering, University of Akron; Research Associate, University of Kansas Museum of Natural History; Research Associate, Carnegie Museum

Bruce M Rothschild, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Rheumatology, International Skeletal Society, New York Academy of Sciences, Sigma Xi, Society of Skeletal Radiology

Disclosure: Nothing to disclose.

Coauthor(s)

Michael A Bruno, MD, MS, FACR Professor of Radiology and Medicine, Pennsylvania State University College of Medicine; Director, Radiology Quality Management Services, The Penn State Milton S Hershey Medical Center

Michael A Bruno, MD, MS, FACR is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, Association of University Radiologists, Radiological Society of North America, Society of Nuclear Medicine and Molecular Imaging, Society of Skeletal Radiology

Disclosure: Received royalty from Oxford Press for book author/editor & reviewer; Received royalty from Elsevier Press for book author / editor.

Specialty Editor Board

Bernard D Coombs, MB, ChB, PhD Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand

Disclosure: Nothing to disclose.

Theodore E Keats, MD Professor, Departments of Radiology and Orthopedics, University of Virginia School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Felix S Chew, MD, MBA, MEd Professor, Department of Radiology, Vice Chairman for Academic Innovation, Section Head of Musculoskeletal Radiology, University of Washington School of Medicine

Felix S Chew, MD, MBA, MEd is a member of the following medical societies: American Roentgen Ray Society, Association of University Radiologists, Radiological Society of North America

Disclosure: Nothing to disclose.

Acknowledgements

Hussein M Abdel-Dayem, MD Professor of Radiology, New York Medical College

Disclosure: Nothing to disclose.

References
  1. Jones AC, Chuck AJ, Arie EA. Diseases associated with calcium pyrophosphate deposition disease. Semin Arthritis Rheum. 1992 Dec. 22(3):188-202. [Medline].

  2. Rothschild BM, Martin LD. Calcium pyrophosphate Deposition Disease. Rothschild BM, Martin LD. SKeletal Impact of Disease. 1st. Albuquerque, NM: New Mexico Museum of Natural History; 2006.

  3. Tsui FW. Genetics and mechanisms of crystal deposition in calcium pyrophosphate deposition disease. Curr Rheumatol Rep. 2012 Apr. 14(2):155-60. [Medline].

  4. Miksanek J, Rosenthal AK. Imaging of calcium pyrophosphate deposition disease. Curr Rheumatol Rep. 2015 Mar. 17 (3):20. [Medline].

  5. Zhang W, Doherty M, Bardin T, Barskova V, Guerne PA, Jansen TL, et al. European League Against Rheumatism recommendations for calcium pyrophosphate deposition. Part I: terminology and diagnosis. Ann Rheum Dis. 2011 Apr. 70(4):563-70. [Medline].

  6. Tan KB, Scolyer RA, McCarthy SW, Schatz J, Nabarro M, Lee K, et al. Tumoural calcium pyrophosphate dihydrate crystal deposition disease (tophaceous pseudogout) of the hand: a report of two cases including one with a previously unreported associated florid reactive myofibroblastic proliferation. Pathology. 2008 Dec. 40(7):719-22. [Medline].

  7. Rothschild BM. Distinguishing erosive osteoarthritis and calcium pyrophosphate deposition disease. World J Orthop. 2013 Apr 18. 4(2):29-31. [Medline]. [Full Text].

  8. Barskova VG, Kudaeva FM, Bozhieva LA, Smirnov AV, Volkov AV, Nasonov EL. Comparison of three imaging techniques in diagnosis of chondrocalcinosis of the knees in calcium pyrophosphate deposition disease. Rheumatology (Oxford). 2013 Jun. 52 (6):1090-4. [Medline].

  9. Kaushik S, Erickson JK, Palmer WE. Effect of chondrocalcinosis on the MR imaging of knee menisci. AJR Am J Roentgenol. 2001 Oct. 177(4):905-9. [Medline].

  10. Major NM, Helms CA, Genant HK. Calcification demonstrated as high signal intensity on T1-weighted MR images of the disks of the lumbar spine. Radiology. 1993 Nov. 189(2):494-6. [Medline].

  11. Magarelli N, Amelia R, Melillo N, Nasuto M, Cantatore F, Guglielmi G. Imaging of chondrocalcinosis: calcium pyrophosphate dihydrate (CPPD) crystal deposition disease -- imaging of common sites of involvement. Clin Exp Rheumatol. 2012 Jan-Feb. 30(1):118-25. [Medline].

  12. Ciapetti A, Filippucci E, Gutierrez M, Grassi W. Calcium pyrophosphate dihydrate crystal deposition disease: sonographic findings. Clin Rheumatol. 2008 Nov 13. [Medline].

  13. Fodor D, Albu A, Gherman C. Crystal-associated synovitis- ultrasonographic feature and clinical correlation. Ortop Traumatol Rehabil. 2008 Mar-Apr. 10(2):99-110. [Medline].

  14. Newman JS, Laing TJ, McCarthy CJ. Power Doppler sonography of synovitis: assessment of therapeutic response--preliminary observations. Radiology. 1996 Feb. 198(2):582-4. [Medline].

  15. Sofka CM, Adler RS, Cordasco FA. Ultrasound diagnosis of chondrocalcinosis in the knee. Skeletal Radiol. 2002 Jan. 31(1):43-5. [Medline].

  16. Gutierrez M, Di Geso L, Salaffi F, Carotti M, Girolimetti R, De Angelis R, et al. Ultrasound detection of cartilage calcification at knee level in calcium pyrophosphate deposition disease. Arthritis Care Res (Hoboken). 2014 Jan. 66 (1):69-73. [Medline].

  17. Filippou G, Filippucci E, Tardella M, et al. Extent and distribution of CPP deposits in patients affected by calcium pyrophosphate dihydrate deposition disease: an ultrasonographic study. Ann Rheum Dis. 2013 Mar 26. [Medline].

  18. Mizutani H, Ohba S, Mizutani M. Tumoral calcium pyrophosphate dihydrate deposition disease with bone destruction in the shoulder. CT and MR findings in two cases. Acta Radiol. 1998 May. 39(3):269-72. [Medline].

  19. Chen C, Chandnani VP, Kang HS. Scapholunate advanced collapse: a common wrist abnormality in calcium pyrophosphate dihydrate crystal deposition disease. Radiology. 1990 Nov. 177(2):459-61. [Medline].

  20. Kakitsubata Y, Boutin RD, Theodorou DJ. Calcium pyrophosphate dihydrate crystal deposition in and around the atlantoaxial joint: association with type 2 odontoid fractures in nine patients. Radiology. 2000 Jul. 216(1):213-9. [Medline].

  21. Salaffi F, Carotti M, Guglielmi G, Passarini G, Grassi W. The crowned dens syndrome as a cause of neck pain: clinical and computed tomography study in patients with calcium pyrophosphate dihydrate deposition disease. Clin Exp Rheumatol. 2008 Nov-Dec. 26(6):1040-6. [Medline].

  22. Stucki G, Hardegger D, Bohni U. Degeneration of the scaphoid-trapezium joint: a useful finding to differentiate calcium pyrophosphate deposition disease from osteoarthritis. Clin Rheumatol. 1999. 18(3):232-7. [Medline].

 
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Anteroposterior radiograph of knee. Radiodense lines paralleling the articular surface and calcification in the menisci of the knee identify the presence of chondrocalcinosis.
Magnified anteroposterior radiograph of knee demonstrating chondrocalcinosis within the meniscal cartilage of the knee.
Anteroposterior radiograph of navicular cysts. These cysts are not specific for calcium pyrophosphate deposition disease. They may be posttraumatic or ganglion cysts.
Crumbling-type erosions of calcium pyrophosphate deposition disease in the metacarpophalangeal and proximal and distal interphalangeal joints. A: Dorsal view of metacarpophalangeal joints with a smudged appearance. B: Anteroposterior radiograph of metacarpophalangeal 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.
Spine involvement in calcium pyrophosphate deposition disease. A: Anterior view of lumbar spine. Apparent bridging is not associated with erosions at the anterosuperior and anteroinferior borders of the vertebral bodies (in contrast to that seen in spondyloarthropathy). B: Lateral radiograph of lumbar spine with calcification of vertebral disks.
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.
Posteroanterior radiograph of the wrist. Note the chondrocalcinosis of the triangular fibrocartilage (TFCC) and indentation of the radiocarpal joint.
Calcium pyrophosphate deposition disease of the wrist. Again, note calcification within the substance of the triangular fibrocartilage (TFCC) 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).
Oblique view of the surface of the distal radius. Note the indentation of the radiocarpal joint.
Table 1. Distribution Pattern (%) of Nonerosive Component of Primary CPDD in Skeletal and Clinical Populations
Joint Skeletal, % Clinical, %
Knee 54 41-99
Shoulder 38 16-50
Radiocarpal 35 6-43
Metacarpophalangeal 30 19-50
Elbow 24 23-33
Proximal interphalangeal 21 19
Distal interphalangeal 18 19
Hip 16 18-27
Metatarsophalangeal 13 2
Ankle 10 7-11
Interphalangeal 4 2
Table 2. Joint Distribution Pattern (%) of CPDD in Familial, Idiopathic, and Metabolic (eg, hemochromatosis [hemo] and ochronosis [ochro]) Varieties
Joint Familial, %  



Idiopathic, %



Metabolic



Hemo, %



 



Metabolic



Ochro, %



Knee 62 41-99 89 63-99
Radiocarpal 24 6-43 100 3-29
Shoulder 19 16-50 0 49-86
Elbow 14 23-33 11 9-29
Hip 10 18-27 0 43-57
Metatarsophalangeal 8-10 2 0 0
Metacarpophalangeal 5-14 40-50 44 29
Ankle 0-15 7-11 33 0
Spine 0-15 1-17 0-15 100
Table 3. Distribution Pattern (%) of Erosions in Patients With Primary CPDD
Joint Erosions, %
Proximal interphalangeal 12
Metacarpophalangeal 10
Distal interphalangeal 10
Shoulder 9
Metatarsophalangeal 6
Radiocarpal 2
Knee 2
Interphalangeal 2
Elbow 1
Ankle 1
Hip 0
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