Calcium Pyrophosphate Dihydrate Crystal Deposition in and around the Atlantoaxial Joint: Association with Type 2 Odontoid Fractures in Nine Patients

Radiology ◽  
2000 ◽  
Vol 216 (1) ◽  
pp. 213-219 ◽  
Author(s):  
Yousuke Kakitsubata ◽  
Robert D. Boutin ◽  
Daphne J. Theodorou ◽  
Roger M. Kerr ◽  
Lynne S. Steinbach ◽  
...  
2008 ◽  
Vol 8 (1) ◽  
pp. 22-29 ◽  
Author(s):  
Albert J. Fenoy ◽  
Arnold H. Menezes ◽  
Kathleen A. Donovan ◽  
Stephen F. Kralik

Object Calcium pyrophosphate dihydrate (CPPD) deposition is a rare cause of retroodontoid mass lesions in elderly individuals. However, this condition may be severely underdiagnosed if sufficient attention is not paid to imaging characteristics and clinical presentation. The authors sought to evaluate the decision-making process in both the diagnosis and surgical treatment of CPPD. Methods A retrospective review of University of Iowa medical records and radiographs accumulated between 1977 and 2006 was performed. The inclusion criterion was histopathological findings consistent with pseudogout at the craniovertebral junction (CVJ). Twenty-one patients with a mean age of 70.3 years and a mean symptom duration prior to presentation of 17.5 months were identified and included in this study. Results The patients presented most frequently with occipital and neck pain (85%) and numbness or paresthesias (61%). Lower cranial nerve deficits were seen in 29%. Calcification of the mass or transverse ligament was seen on computed tomography in all included patients. Gross-total resection was achieved in all patients: 19 of 21 patients underwent transoral–transpalatopharyngeal resection, with only 16 requiring concomitant dorsal occipital–cervical fusion. The mean follow-up duration was 15 months. Eighteen patients (86%) had improvement or resolution of symptoms after treatment, and 3 were lost to follow-up. Conclusions Although rare, CPPD deposition at the CVJ should be suspected on finding calcification of and around the transverse ligament on neuroimaging. Transoral–transpalatopharyngeal resection is preferred to halt the progression of neurological deterioration; dorsal fusion is not always mandatory as concomitant ligamentous calcification and atlantoaxial joint ankylosis may provide added stability.


Hand Surgery ◽  
2013 ◽  
Vol 18 (03) ◽  
pp. 413-415 ◽  
Author(s):  
Takuma Wakasugi ◽  
Ritsuro Shirasaka ◽  
Hiroaki Kimura ◽  
Yoshiaki Wakabayashi

We report a case of closed rupture of the flexor tendons of the little finger caused by calcium pyrophosphate dihydrate crystal deposition disease of the pisotriquetrum joint. The patient could not flex the little finger and did not have wrist pain. Plain radiographs of the affected wrist joint showed severe arthritic changes of the pisotriquetrum joint and calcification around the joint. At operation, the pisotriquetrum joint capsule was ruptured and involved the flexor tendon of the little finger. The distal stump of the flexor tendon was transferred to the flexor tendon of the ring finger, and the pisiform was resected. Histological examination with polarized light microscopy revealed crystals showing weakly positive birefringence in the calcification.


2019 ◽  
Author(s):  
N Lawrence Edwards

The destructive potential of intracellular crystals has been recognized for over a century. The mechanisms by which crystals induce inflammation and bone and cartilage destruction have been elucidated over the past decade. The three most common crystal-induced arthropathies are caused by precipitation of monosodium urate monohydrate, calcium pyrophosphate dihydrate (CPP) and basic calcium phosphate. The definition, epidemiology, pathogenesis and etiology, diagnosis, and treatment of gout and CPP crystal deposition are reviewed, as well as the clinical stages of gout (i.e., acute gouty arthritis, intercritical gout, advanced gout, nonclassic presentations of gout, and other conditions associated with gout). Also reviewed are the clinical manifestations of calcium pyrophosphate dihydrate deposition disease (CPPD), such as asymptomatic CPPD, osteoarthritis with CPPD, acute CPP crystal arthritis, and chronic CPP crystal inflammatory arthritis. Figures illustrate renal transport of urate, monosodium urate crystals, acute gouty flare, advanced gouty arthritis, gouty synovial fluid, radiographic changes of advanced gout, ultrasound appearance of the femoral intercondylar cartilage, pharmacologic management of gout, the effect of gender and age on knee chondrocalcinosis, radiographs of chondrocalcinosis, and compensated polarized microscopy of CPPD. Tables present the major factors responsible for hyperuricemia, characteristics of classic gouty flares, antiinflammatory therapy for gout, and urate-lowering therapy. This chapter contains 90 references. This review contains 11 figures, 12 tables, and 88 references. Keywords: acute gouty arthritis, intercritical gout, advanced gout, asymptomatic CPPD, osteoarthritis with CPPD, acute CPP crystal arthritis, chronic CPP crystal inflammatory arthritis


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