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PubMed2002

Idiopathic widespread calcium pyrophosphate dihydrate crystal deposition disease in a young patient.

We report a case of generalized chondrocalcinosis in a 34-year-old man with no familial or medical history of associated diseases. Radiographs revealed calcification of the articular cartilages of the limbs, the fibrous rings around the intervertebral disks, the triangular cartilages of the wrists, and the pubic symphysis. On the basis of the presence of calcium pyrophosphate in the synovial fluid of his right ankle and generalized chondrocalcinosis, the patient was diagnosed with idiopathic calcium pyrophosphate dihydrate (CPPD) crystal deposition disease. Nonsteroidal anti-inflammatory drugs and steroid treatment provided symptomatic relief.

Adult↗
PubMed2002

Bilateral symptomatic synovial cysts of the lumbar spine caused by calcium pyrophosphate deposition disease: a case report.

STUDY DESIGN: A case of bilateral symptomatic facet joint synovial cysts arising in association with calcium pyrophosphate deposition disease is reported. OBJECTIVE: To present a previously unreported cause for symptomatic synovial cysts of the lumbar spine. SUMMARY OF BACKGROUND DATA: Synovial cysts of the facet joints occur most commonly in association with degenerative disease of the spine in older individuals. The association of these cysts with trauma, rheumatoid arthritis, spondylolysis, and kissing spinous processes also has been reported. These cysts can cause symptoms and signs from direct compression of the dura. Chondrocalcinosis has not been previously reported to cause symptomatic synovial cysts. METHODS: A 67-year-old woman presented with right lower limb sciatica caused by a right L4-L5 facet joint cyst, which resolved after surgical decompression. A year later, she presented with left lower limb sciatica caused by development of a new L4-L5 facet joint cyst, which also resolved after surgical decompression. RESULTS: Histopathologic examination of each cyst showed a cyst wall of fibrous tissue with synovial lining, inflammation, and granulation tissue. Examination of the tissue under polarized light showed positively birefringent, short blunt crystals of calcium pyrophosphate dihydrate. CONCLUSIONS: In patients with a history of gout or pseudogout, a rare possibility of a synovial cyst should be considered in the differential diagnosis during investigation for the cause of neural compression resulting in sciatic syndrome.

Aged↗
PubMed1975

A phlogistic function of PGE1 in calcium pyrophosphate dihydrate crystal-induced inflammation.

Promotion of calcium pyrophosphate dihydrate (CaPPD) crystal-induced inflammation by prostaglandin (PG) E1 has been demonstrated by two new techniques: (1) Rats deficient in essential fatty acids, biological precursors of PG, developed less footpad swelling than did normal rats following injections of unheated CaPPD. Addition of one ng of PGE1 to these crystals resulted in normal swelling. (2) This phlogistic effect of PGE1 was also demonstrated in normal rats fed a normal dietwho received injections of CaPPD crystals heated to 200 degrees C for three hours. The heated crystals induced less footpad swelling than did unheated crystals. When one ng of PGE1 was added to the suspensions of heated crystals the resultant swelling approximated that obtained by unheated crystals. The possible role of PGE1 in mediating CaPPD crystal-induced inflammation is suggested. An analysis of urate and CaPPD crytal-induced inflammation is presented with comments setting forth the concept that these metabolic crystal disorders are membrane diseases.

Animals↗
PubMed1994

Causal link between nucleotide pyrophosphohydrolase overactivity and increased intracellular inorganic pyrophosphate generation demonstrated by transfection of cultured fibroblasts and osteoblasts with plasma cell membrane glycoprotein-1. Relevance to calcium pyrophosphate dihydrate deposition disease.

OBJECTIVE: In subjects with idiopathic calcium pyrophosphate dihydrate (CPPD) deposition disease, cartilage chondrocytes elaborate increased amounts of PPi. The mechanism of the intracellular PPi elevation is not known. Plasma membrane 5'-nucleotide phosphodiesterase I/nucleotide pyrophosphohydrolase (NTPPPH) activity also is elevated in chondrocytes and dermal fibroblasts of patients with idiopathic CPPD deposition disease. NTPPPH, as an ecto-enzyme, could act within certain intracellular compartments. Thus, we hypothesized a potential causal link between increased NTPPPH activity and increased intracellular PPi. METHODS: Transformed simian fibroblasts (COS cells) and human osteoblasts (U2OS cells) were transfected with the 5'-nucleotide phosphodiesterase I ecto-enzyme plasma cell membrane glycoprotein-1 (PC-1), recently shown to be expressed in cartilage, osteoblasts, and fibroblasts. RESULTS: Transfection with PC-1 markedly up-regulated 5'-nucleotode phosphodiesterase I activity and increased intracellular PPi concentrations by increasing the capacity of cells to generate PPi. Importantly, this did not require supplementation with exogenous nucleotides. CONCLUSION: Cellular overexpression of PC-1 produces NTPPPH overactivity and increased intracellular PPi generation in vitro. These findings support the potential importance of NTPPPH overactivity in PPi generation, both inside and outside the cell, in some subjects with CPPD deposition disease.

Animals↗
PubMed1998

Calcium pyrophosphate deposition disease of the temporal bone.

Massive calcium pyrophosphate crystal deposition is a rare disorder that may affect the temporomandibular joint and temporal bone. The diagnosis is difficult, and misdiagnosis as malignancy, particularly chondrosarcoma, is frequent. This can lead to unnecessarily aggressive management. The clinical, radiographic, and pathologic features of this entity are reviewed, and treatment options are discussed.

Aged↗
PubMed1995

Calcium pyrophosphate dihydrate crystal deposition disease in the elderly.

Calcium pyrophosphate dihydrate deposition disease can mimic a large number of joint diseases. We report on three patients with predominantly systemic symptoms. Diagnostic pitfalls and treatment delays in these patients are discussed. Once the diagnosis is considered, confirmation is readily obtained by examination of the joint fluid and treatment promptly relieves symptoms.

Aged↗
PubMed1977

Clinical, radiographic and pathologic abnormalities in calcium pyrophosphate dihydrate deposition disease (CPPD): pseudogout.

Clinical, radiographic and pathologic abnormalities in calcium pyrophosphate dihydrate deposition disease (CPPD) (pseudogout) are outlined in an investigation of 85 patients with definite or probable disease and available cadaveric and human surgical material. Pyrophosphate arthropathy produced distinctive roentgenographic abnormalities with were most frequent in the knee, wrist and metacarpophalangeal joints. Although the alterations superficially resembled osteoarthritis, they were frequently more severe and progressive with extensive fragmentation of bone, causing intra-articular osseous bodies. Pyrophosphate arthropathy occurred in unusual locations, such as the radiocarpal compartment of the wrist, elbow, and patellofemoral compartment of the knee. These characteristics allow the radiologist to suggest a probable diagnosis of CPPD even in the absence of articular calcification.

Aged↗
PubMed1988

Calcium pyrophosphate crystal deposition: the effect of monosodium urate and apatite crystals in a kinetic study using a gelatin matrix model.

The kinetics of calcium pyrophosphate dihydrate (CPPD) crystal growth was studied by allowing calcium and pyrophosphate (PPi-4) ions to diffuse through a denatured collagen matrix (biological grade gelatin) in the presence of either monosodium urate monohydrate (MSU) or hydroxyapatite (HA) crystals. In this in vitro model system, MSU crystals significantly altered the kinetics of PPi-4 ionic diffusion through the gelatin matrix by allowing the [PPi-4] gradient to fall off much more rapidly, suggesting an increased level of scavenging of PPi-4 ions into crystalline materials. Even more significantly, the presence of MSU crystals markedly influenced the crystal growth morphology of triclinic CPPD, producing that observed in vivo. A large number of epitaxially dimensional matches between MSU and triclinic (t) and monoclinic (m) CPPD were identified, suggesting that MSU crystals can epitaxially induce CPPD crystal growth. This finding supports the hypothesis that the association of urate gout and CPPD crystal deposition disease is based on the nucleating potential of MSU crystals for CPPD crystal growth. In contrast, the HA crystal structure did not appear to serve as a nucleating agent for CPPD crystals. However, HA crystals did serve as effective traps for PPi-4 ions and their presence led to more stable CPPD crystal growth.

Apatites↗
PubMed1988

Deposition of calcium pyrophosphate dihydrate crystals in the hand.

A rare case with deposition of calcium pyrophosphate dihydrate crystals around the proximal portion of the first and second metacarpal bones is reported. The second metacarpal had a cystic lesion, and the cortex of the first metacarpal had irregular osteolytic change. There were degenerative changes in the first carpometacarpal joint, trapeziotrapezoid articulation, and second carpometacarpal joint. The patient had recurrent acute inflammatory attacks at the affected site. Initially the patient was thought to have tumoral calcinosis, or a calcifying soft-tissue tumor, with the possibility of a malignant tumor because of angiographic evidence of tumor stain and hypervascularity. Surgical biopsy with partial curettage of the calcified mass resulted in early recurrence of deposition of the crystals. Total excision would seem to be necessary to avoid recurrence.

Calcium Pyrophosphate↗
PubMed1988

Massive solitary tophus containing calcium pyrophosphate dihydrate crystals at the acromioclavicular joint.

A massive solitary tophus containing calcium pyrophosphate dihydrate (CPPD) crystals was resected from the distal clavicle and proximal acromion of a 62-year-old man who presented with a painful shoulder mass. The diagnosis was confirmed histologically and by X-ray diffraction. CPPD crystal deposition was found within bone, however, the articular cartilage was not involved. Other unusual features of the case include the size of the lesion, the monoarticular presentation and a peculiar discoloration of the overlying skin. The clinical presentation and radiographic features were initially consistent with a malignant process; thus the case demonstrates that CPPD arthropathy should be included in the differential diagnosis of periarticular tumors.

Acromioclavicular Joint↗
PubMed1996

Tumoral calcium pyrophosphate dihydrate deposition disease: cytopathologic findings on fine-needle aspiration.

Tumoral calcium pyrophosphate dihydrate deposition disease (CPPD) is a rare non-neoplastic entity which mimics primary or metastatic soft-tissue or skeletal malignancy. Fewer than a dozen cases have been reported in the literature with only histologic descriptions. We present cytologic findings of a unique case of CPPD in a 73-year-old black female with a history of end-stage renal disease. A fine-needle aspiration (FNA) was done on a 4 x 4-cm neck mass which was clinically thought to be malignant. Cytopathologic examination showed numerous macrophages with markedly distended cytoplasm and containing multiple yellowish-orange, short rhomboid crystals. These were strongly birefringent on polarized microscopy, consistent with CPPD crystals.

Aged↗
PubMed2005

Monosodium urate and calcium pyrophosphate dihydrate (CPPD) crystals, inflammation, and cellular signaling.

Monosodium urate (MSU) and calcium pyrophosphate dihydrate (CPPD) crystals are responsible for acute synovial inflammation but also contribute to cartilage degradation and bone lesions within the joint. They activate multiple signal transduction pathways leading to cell activation and recruitment. Some signalling pathways are activated by both types of crystals, and other pathways may only be activated by one type depending on cell type, namely neutrophils, monocytes, macrophages, synovial fibroblasts, endothelial cells and chondrocytes. Cascades of activated proteins involve cytoplasmic membrane related proteins (FAK complex, Src family tyrosine kinases), but also MAPK and NF-kB pathways, leading to NO, prostanoid and cytokine production, and protease activation. This review will also focus on potential therapeutic targets related to cellular signalling in MSU and CPPD crystal-induced inflammation.

Animals↗
PubMed1981

Clearance of calcium pyrophosphate dihydrate crystals in vivo. III. Effects of synovial hemosiderosis.

Synthetic triclinic calcium pyrophosphate dihydrate crystals, uniformly labeled with 85Sr and 45Ca, were injected into the knee joints of 2 normal adult rabbits and 2 rabbits previously injected repeatedly with autologous blood. The "half clearance time" of the injected crystal mass was 20.4 and 19 days from control joints, nearly identical to previously reported values in 6 rabbits (19.1 +/- 1.4), and 28.8 and 34 days from the joints injected with blood, a significant difference (P less than 0.05). Iron stains showed hemosiderin granules in the superficial synovium in these joints. Electron microscopy showed crystals with a molar calcium/phosphorus ratio of 1.0 and particles containing iron within synovial cells. We hypothesize that the decreased clearance rate from hemosiderotic synovium is due to inhibition of one or more intracellular pyrophosphatases by iron.

Animals↗
PubMed2026

Co-occurrence of rheumatoid arthritis and calcium pyrophosphate deposition disease: A systematic literature review.

BACKGROUND: Rheumatoid arthritis (RA) and calcium pyrophosphate deposition (CPPD) disease are forms of inflammatory arthritis which may have similar presentations. There is growing recognition that these conditions can coexist, especially in elderly patients. This systematic literature review aims to examine the epidemiology and clinical characteristics of patients with both RA and CPPD disease. METHODS: A systematic literature search was performed from database inception to 31st January 2026 using the databases EMBASE, MEDLINE, Scopus, PubMed, CINAHL, and Cochrane. Keywords relating to RA, CPPD and chondrocalcinosis were used. Inclusion criteria were studies published in English and those that addressed the co-occurrence of RA and CPPD. RESULTS: The search yielded 24 studies comprising 12 cross-sectional studies, 2 case series, and 10 case reports published between 1965 and 2026. A total of 404 patients had both RA and CPPD, with 397/404 (98.3%) aged over 60 years old. Of 365 patients with serostatus data, 204/339 (60.2%) were seronegative for both rheumatoid factor (RF) and anti-citrullinated protein antibody (ACPA). Radiographic chondrocalcinosis was evident in 271/287 (94.4%). Of 271 patients with chondrocalcinosis, 162 (59.8%) were seronegative for both RF and ACPA. The most prescribed medications were methotrexate and prednisolone, in 75/205 (36.6%) and 64/205 (31.2%) patients, respectively. Colchicine was prescribed for 24/205 (11.7%). CONCLUSION: While the studies were small, RA, which is commonly seronegative, and CPPD can co-exist in the elderly. Higher-quality studies are required to determine the prevalence of co-existent RA and CPPD, thereby improving insight into the epidemiology and potentially enhancing outcomes of these patients.

Humans↗
PubMed1975

Calcium pyrophosphate dihydrate deposition disease without chondrocalcinosis.

The pseudogout syndrome is usually associated with radiographic evidence of articular cartilage calcification. Eight patients who had joints containing calcium pyrophosphate dihydrate crystals were studied. Extensive radiographic evaluation was obtained in seven patients and a limited evaluation in the other. None had evidence of chondrocalcinosis. Six had distinctive radiographic abnormalities of the wrists consisting of radiocarpal joint space narrowing and sclerosis, and subchondral cystic degeneration of the carpal bones. We conclude that calcium pyrophosphate dihydrate deposition disease and pseudogout can occur without radiographic evidence of chondrocalcinosis and that the diagnosis can be suggested by characteristic radiographic abnormalities of the wrists.

Adult↗
PubMed1979

CLearance of calcium pyrophosphate dihydrate crystals in vivo. II. Studies using triclinic crystals doubly labeled with 45Ca and 85Sr.

The clearance rate of isotopically labeled synthetic triclinic calcium pyrophosphate dihydrate (CPPD) crystals injection into rabbit joints was estimated by serial counting. Kinetic analysis using a four compartment model showed that half of the injected dose was cleared from 4 rabbit knee joints in 19.1 +/- 0.42 (SEM) days. Profound hypomagnesemia, produced in 2 rabbits with a low magnesium diet, did not affect the rate of crystal clearance detectably. Lavage of joints with solutions known to promote CPPD crystal solubility failed to remove detectable radioactivity. The previous finding of CPPD crystals in synovial phagocytes by electron microscopy, together with the finding of nuclide activity in the synovium and the failure to remove such activity by joint lavage, suggests that endocytosis by synovial cells is an important, effective mechanism controlling the synovial fluid concentration of crystals in patients with CPPD crystal deposition disease.

Animals↗
PubMed1988

Inhibition of calcium pyrophosphate dihydrate crystal formation: effects of carboxylate ions.

Proteoglycans are recognized to inhibit calcium pyrophosphate dihydrate (CPPD) crystal formation but the mechanisms are not known. To study the role of carboxylate (-CO2-) ligands, the possible inhibitor effects of sodium acetate, sodium D-glucuronate, disodium malate, and trisodium citrate were studied using solution mixtures containing [Ca2+] = 1.5 mM, [Mg2+] = 0.5 mM, [PPi] = 0.1 mM, [Pi] = 0.1 mM, [Na+] = 140 mM, 37 degrees C, pH 7.4 with or without 9.5 +/- 0.5 mg CPPD (seed) crystals. These studies showed that monocarboxylates (acetate, glucuronate) have little inhibitive effect. Progressively greater inhibition was found with dicarboxylate (malate) and tricarboxylate (citrate) indicating that the arrangement of carboxylate (and sulfate) ligands on proteoglycan is more important than the inhibitory effect of individual ligands.

Calcium↗
PubMed1999

Most calcium pyrophosphate crystals appear as non-birefringent.

OBJECTIVE: To determine the proportion of calcium pyrophosphate dihydrate (CPPD) crystals that appear as non-birefringent when observed under the polarised light microscope. METHODS: Two observers examined independently 10 synovial fluid samples obtained during an episode of arthritis attributable to CPPD crystals. Ten synovial fluid samples from patients with acute gout were used as a reference. The examination was performed after placing a fluid sample in a Niebauer haemocytometric chamber; a crystal count was done first under ordinary light, then in the area corresponding to a 0.1 ml, under polarised light RESULTS: The percentages of birefringence appreciated for CPPD were 18% (confidence intervals (CI) 12, 24) for observer 1, and 17% (CI 10, 24) for observer 2 (difference NS). The percentages of birefringence for monosodium urate were 127% (CI 103, 151) for observer 1 and 107% (CI 100, 114) for observer 2 (difference NS). Percentages above 100% indicate that crystals missed under ordinary light became apparent under polarised light. CONCLUSION: Only about one fifth of all CPPD crystals identified by bright field microscopy show birefringence when the same synovial fluid sample is observed under polarised light. If a search for CPPD crystals is conducted under polarised light, the majority of the crystals will be missed. Ordinary light allows a better rate of CPPD crystal detection but observation under polarised light of crystals showing birefringence is required for definitive CPPD crystal identification.

Birefringence↗