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At least 199 records · Page 11Linked to original sources
PubMed2000

Retro-odontoid massive calcium pyrophosphate crystal deposition--case report.

An 86-year-old male presented with progressive myelopathy due to retro-odontoid massive deposits of calcium pyrophosphate dihydrate (CPPD) crystals. Magnetic resonance imaging revealed a non-enhanced isointense extradural mass on the T1-weighted image and heterogeneously intense mass on the T2-weighted image. Computed tomography showed typical punctate and linear calcifications within the mass. The mass was resected via a lateral approach resulting in marked improvement of the symptoms. Histological examination revealed birefringent rhomboid crystals consistent with CPPD. CPPD deposition should be considered in the differential diagnosis of retro-odontoid extradural mass because surgical therapy is beneficial even for elderly patients.

Aged↗
PubMed2003

Mutations in the amino terminus of ANKH in two US families with calcium pyrophosphate dihydrate crystal deposition disease.

OBJECTIVE: To analyze ANKH in families with calcium pyrophosphate dihydrate crystal deposition disease (CPPD) for disease-causing mutations. METHODS: Two US families (one of British ancestry and the other of German/Swiss ancestry) with autosomal-dominant CPPD, whose disease phenotypes were found to be linked to chromosome 5p15.1 (locus symbol CCAL2), were screened by direct sequencing for mutations in ANKH, a gene in the CCAL2 candidate interval that has been shown to harbor mutations in other families with CPPD. Observed sequence variants were confirmed by antisense sequencing, and expression of the mutant allele was verified by reverse transcriptase-polymerase chain reaction amplification of messenger RNA followed by direct sequencing. RESULTS: The two US families displayed the same mutation at position 5 of the ANKH gene product (P5T). All affected members were heterozygous for the P-to-T variant, and the mutation was not seen in 204 control alleles. The two families displayed distinct disease haplotypes, suggesting that they were unrelated to each other. CONCLUSION: These observations represent the fourth and fifth families with heritable CPPD whose disease phenotypes are linked to the CCAL2 locus and who have missense mutations in the amino terminus of ANKH. This same position (P5) was the site of a missense mutation in an Argentine family of northern Italian ancestry; however, the sequence variant in that family generated a P5L mutation. The distinct disease haplotypes among the 3 families with P5 mutations suggest that the mutations arose independently and that the evolutionarily conserved P5 position of ANKH may represent a hot spot for mutation in families with autosomal-dominant CPPD.

Chondrocalcinosis↗
PubMed1997

Calcium pyrophosphate dihydrate crystals activate MAP kinase in human neutrophils: inhibition of MAP kinase, oxidase activation and degranulation responses of neutrophils by taxol.

The activation of MAP kinase in human neutrophils stimulated by both uncoated and plasma-opsonized crystals of triclinic calcium pyrophosphate dihydrate (CPPD) was investigated. The effect of taxol on MAP kinase activation and on the responses of neutrophils stimulated by plasma-opsonized crystals was determined. MAP kinase activation was identified and quantified in Mono Q chromatography separated fractions of neutrophils that had been incubated with CPPD crystals by measuring [gamma-32P]adenosine triphosphate (ATP) phosphorylation of myelin basic protein and using immunoblotting techniques. Human neutrophils were incubated with taxol (0-50 microM), added to plasma-opsonized CPPD (50 mg/ml) and MAP kinase activation, chemiluminescence, superoxide anion generation, lysozyme and myeloperoxidase release were monitored. Both uncoated and plasma coated CPPD crystals induced a large increase in MAP kinase activity in neutrophils over control levels within 1 min of incubation. Pretreatment of neutrophils with taxol was able to suppress this activation of MAP kinase. Taxol produced a concentration-dependent inhibition of opsonized CPPD-induced neutrophil chemiluminescence, superoxide anion production and myeloperoxide release. Taxol at 28 microM also significantly inhibited chemiluminescence, superoxide anion production and myeloperoxidase release from neutrophils stimulated by opsonized zymosan. This is the first report of crystal-induced activation of MAP kinase in neutrophils. Microtubule-associated processes, such as signal transduction, secretion and phagocytosis are involved in particulate-induced neutrophil responses. We have suggested that the inhibitory effect of taxol observed in this work is due to its stabilizing effect on microtubules and disruption of MAP kinase activation associated with microtubules.

Antineoplastic Agents, Phytogenic↗
PubMed1984

Low incidence of calcium pyrophosphate dihydrate crystal deposition in rheumatoid arthritis, with modification of radiographic features in coexistent disease.

A negative correlation between rheumatoid arthritis (RA) and calcium pyrophosphate dihydrate (CPPD) crystal deposition was demonstrated in separate controlled radiographic and synovial fluid surveys of RA patients aged 55-75 years. Knee chondrocalcinosis was detected in 14% of 135 normal controls and 28% of 87 post-meniscectomy ("joint damage") controls (P less than 0.05), but only 3% of 100 RA and 75 osteoarthritis patients revealed CPPD crystals in 1% and 23%, respectively (P less than 0.01). Ten subjects with coexistent RA and CPPD deposition were also studied; 7 showed radiographic features atypical of RA, including patchy, asymmetric disease, retained bone density, prominent osteophytosis, well-corticated cysts, and paucity of progressive erosive disease. It is suggested that rheumatoid joint damage, unlike that in osteoarthritis, is not conducive to CPPD crystal formation. When RA and CPPD coexist, atypical radiographic features reflecting a hypertrophic reparative response may occur.

Aged↗
PubMed1990

Synovial fluid calcium pyrophosphate dihydrate crystals and alizarin red positivity: analysis of 3000 samples.

Three thousand synovial fluids (1312 patients: chronic pyrophosphate arthropathy (CPA), 41%; osteoarthritis (OA), 12%; rheumatoid arthritis (RA), 16%) were examined for crystals, including calcium pyrophosphate dihydrate (CPPD), by polarized microscopy (score 0-3); calcific particles, by alizarin red positivity (ARP; 0-3); and total cell count. For 1150 fluids, local joint inflammation was assessed as 'active' or 'inactive' using a summated score of six clinical variables. CPPD and ARP scores did not correlate, but each showed positive correlation with age (P less than 0.01, P less than 0.02 respectively). Pseudogout had the highest mean CPPD score (P less than 0.001); intermittent CPPD positivity (range 8-100%) was seen in serially aspirated CPA joints, and there was no difference in CPPD positivity or score between active and inactive CPA. ARP was most frequent in OA subsets (72% of CPA, 46% of OA, 31% of RA; P less than 0.001). ARP was more frequent in active than inactive OA (P less than 0.05) but showed no association with inflammation in CPA or RA. Cell counts were higher in RA and pseudogout compared to OA and CPA, and in active compared to inactive RA. No correlation was found between ARP or CPPD scores and cell count. Cholesterol crystals were uncommon (0.2%) and showed no disease or joint predilection. In arthritic joints, CPPD and calcific particles particularly associate with the OA process and ageing. CPPD may contribute to acute and other calcific particles to chronic inflammation in OA.

Adolescent↗
PubMed1983

Phagocytosis of hydroxyapatite or calcium pyrophosphate dihydrate crystals by rabbit articular chondrocytes stimulates release of collagenase, neutral protease, and prostaglandins E2 and F2 alpha.

Synthetic hydroxyapatite (HA) and calcium pyrophosphate dihydrate (CPPD) microcrystals are phagocytosed by rabbit articular-cartilage chondrocytes in primary culture. The ingestion of crystals greatly stimulated the release of collagenase, neutral protease, and prostaglandins E2 and F2 alpha into the ambient medium. Lactate dehydrogenase was not released by either crystal despite electron microscopic evidence of cell damage by HA crystals (partial loss of phagolysosomal membrane and increased myelin figures). HA, but not CPPD crystals, stimulated release of beta-glucuronidase. HA crystal concentrations from 50 to 200 micrograms ml-1 induced a dose-dependent release of collagenase and of extracellular protein. Both phagocytosis and collagenase release were greatly attenuated when HA crystals were added to the chondrocyte monolayers in the absence of serum. As HA and CPPD crystals have been identified in human articular cartilage in association with degenerative changes, it is possible that the cell-crystal interaction described here may be pathogenetically important.

Animals↗
PubMed1999

Degeneration of the scaphoid-trapezium joint: a useful finding to differentiate calcium pyrophosphate deposition disease from osteoarthritis.

This study aimed to determine whether osteoarthritis of the scaphoid-trapezium joint (ST osteoarthritis) is associated with calcium pyrophosphate deposition disease (CPDD) in an elderly population with or without concomitant polyarthritis of the finger joints (FIPO). An age- and gender matched case-control study was performed at a university hospital outpatient clinic. Cases and controls were identified from a clinical registry. The case ascertainment process included: (1) chart review for evidence of pyrophosphate crystals from arthrocentesis and/or cartilage calcifications and (2) blinded reading of hand X-rays by three observers for calcification of the triangular fibrocartilage and/or cartilage calcification around the spatium triangulare. Osteoarthritis was graded from 0 to 4 according to the Standard Atlas of Radiographs. The association of ST osteoarthritis with the diagnosis was examined using chi2 tests or the Wilcoxon rank sum test as appropriate. From 65 potential cases, 30 fulfilled the inclusion/exclusion criteria whereas from 185 potential controls, 81 fulfilled the inclusion/exclusion criteria. Thirty controls were matched to cases for gender and age. ST osteoarthritis was much more severe in CPDD (median: 3.0) than in patients with FIPO (median: 0.3) and was strongly associated with the diagnosis (odds ratio 13.8; CI 3.4-59.8). Definite ST osteoarthritis identified CPDD with a sensitivity of 83% and a specificity of 73% with regard to FIPO. It was concluded that the presence of ST osteoarthritis is a helpful diagnostic finding for the diagnosis of CPDD in an elderly, predominantly female population with a high prevalence of FIPO. Especially in cases without radiographic cartilage or fibrocartilage calcification of the wrist, ST osteoarthritis may point to the correct diagnosis.

Aged↗
PubMed1983

Hand and wrist arthropathies of hemochromatosis and calcium pyrophosphate deposition disease: distinct radiographic features.

Radiographic features of hand and wrist involvement in 26 patients with hemochromatosis and in 26 patients with idiopathic calcium pyrophosphate dihydrate (CPPD) crystal deposition disease were compared. Two radiologists independently examined the radiographs without knowledge of the specific group to which the patient belonged. The results of this study clearly establish that structural joint diseases in the two disorders are not identical. Characteristic findings allow the radiologist to favor one diagnosis over the other. These radiographic differences indicate that the arthropathy of hemochromatosis is related to factors additional to the presence of CPPD crystals, specifically, the more prevalent narrowing of the metacarpophalangeal joint spaces, including those in the fourth and fifth digits, peculiar hook-like osteophytes on the radial aspect of the metacarpal heads, and less prevalent separation of the scaphoid and the lunate.

Adult↗
PubMed1993

Calcium pyrophosphate dihydrate crystal deposition disease and pseudogout of the acromioclavicular joint: radiographic and pathologic features.

OBJECTIVE: To correlate the radiographic and pathologic findings in calcium pyrophosphate dihydrate (CPPD) crystal deposition disease and the pseudogout syndrome in the acromioclavicular (AC) joint, a relatively infrequent, but clinically important site. METHODS: We describe a case with a definite diagnosis of CPPD crystal deposition leading to pseudogout of the AC joint. We also identified 17 other patients with CPPD crystal deposition disease who showed intraarticular or periarticular calcification in this joint and investigated the radiographic findings in 26 AC joints in these 17 patients. We then correlated the results with the pathologic findings in 2 cadavers with AC joint manifestations of the disease. RESULTS: Intradiscal calcification, mainly linear or punctate in configuration, was found between adjacent bony margins in 9 of 26 AC joints (35%) or between the bony margins and extending above the upper articular bony margin in 14 AC joints (54%). Two joints (8%) showed diffuse calcification within the discs between, above, and below the articular bony margins. The remaining joint (3%) had intradiscal calcification only above the upper bony margins of the AC joint. All the joints with calcifications above the articular margins had associated globular or tumor-like soft tissue masses. A pseudogout attack at the AC joint may have nonspecific shoulder pain as its presenting symptom. CONCLUSION: CPPD crystal deposition disease leading to pseudogout syndrome of the AC joint is a clinically significant condition. We emphasize that careful assessment of the AC joint and adjacent soft tissue using intensive bright light on routine shoulder radiographs may increase the sensitivity of detecting discal and capsular calcifications in patients with pseudogout of the shoulder.

Acromioclavicular Joint↗
PubMed2001

Diff Quik staining method for detection and identification of monosodium urate and calcium pyrophosphate crystals in synovial fluids.

OBJECTIVE: To evaluate whether the Diff Quik (DQ) staining method might prove useful in identifying monosodium urate (MSU) and calcium pyrophosphate dihydrate (CPPD) crystals on permanent mounted stained slides. METHODS: 27 synovial fluid (SF) samples obtained from the knees of 21 patients with acute CPPD disease and 6 with acute gout were studied. Wet analysis for crystal detection and identification was performed within one hour of joint aspiration. In addition, 16 inflammatory synovial effusions obtained from patients with knee arthritis induced by non-crystalline inflammatory diseases were studied. For each SF, a DQ stained slide was analysed by two of the authors trained in SF analysis. The observers were blinded to the type of crystals present in the SF. Each slide was analysed by compensated polarised as well as transmitted light microscopy. An SF was considered positive if intracellular and/or extracellular crystals were clearly identified. In addition, the observer was asked to identify the type of the crystals using compensated polarised light microscopy. Sensitivity, specificity, accuracy, positive predictive value (PPV), and negative predictive value (NPV) of the DQ staining method were determined. RESULTS: 51 true positive and 28 true negative cases were correctly classified (39 CPPD samples, 12 MSU samples, 28 samples of crystal unrelated arthropathies). Overall, four false positive and three false negative cases were reported. In all the false positive cases, extracellular CPPD crystals were erroneously identified, whereas CPPD crystals present in the SF were not identified in the three false negative cases. All MSU specimens were correctly diagnosed. The overall specificity, sensitivity, and accuracy using DQ stained slides for crystal confirmation were respectively 87.5%, 94.4%, and 91.9%. The PPV was 92.7% and the NPV 90.3%. In particular, the specificity, sensitivity, and accuracy for CPPD detection were 90.9%, 92.9%, and 91.9%, with a PPV of 90.7 and an NPV of 93.0%. All the MSU specimens were correctly identified, providing 100% sensitivity, specificity, accuracy, PPV, and NPV. CONCLUSIONS: Stained preparations of SF, including DQ stained smears, could provide a useful tool for delayed SF analysis suitable for quality controls, including cytological examination and crystals detection and identification.

Benchmarking↗
PubMed2000

[Mixed tophi. Calcium pyrophosphate dihydrate crystals in gout tophi].

Calcification of tophi is a well-known secondary phenomenon in gout. Because there are no data available on the nature of the calcium component, light and scanning electron microscopic as well as X-ray microanalysis studies were performed on calcified tophi. In unstained histological slides, urate crystals were detected as negative birefringent needles; after incubation of the slides in distilled water, the urate crystals had disappeared, only positive birefringent calcium pyrophosphate dihydrate (CPPD) crystals of different size remained. An identical result was obtained by scanning electron microscopy. By X-ray microanalysis, peaks for calcium and phosphorus were measured, indicating the presence of CPPD. The occurrence of CPPD crystals in urate tophi as well as in foreign body granulomata indicates that the occurrence of CPPD is not restricted to articular tissues. The biochemical mechanism leading to the appearance of these crystals remains unknown, but it may be assumed that an increase of connective tissue destruction may be responsible for this calcification process.

Adult↗
PubMed1977

Carpal instability in rheumatoid arthritis and calcium pyrophosphate deposition disease. Pathogenesis and roentgen appearance.

The roentgen appearance and pathogenesis of carpal instability are described in an evaluation of patients and cadavers with rheumatoid arthritis and calcium pyrophosphate deposition disease. Dorsiflexion (16%) and palmar flexion (8%) instability occurs in rheumatoid arthritis, particularly in patients with moderate to advanced disease. Navicular-lunate dissociation frequently accompanies dorsiflexion instability and results from involvement of the interosseous ligament between the two bones by rheumatoid pannus. Carpal instability and navicular-lunate dissociation also accompany pyrophosphate arthropathy, resulting from calcific deposition and cystic degeneration of ligamentous structures.

Adult↗
PubMed1984

Transmission electron microscopic identification of silicon-containing particles in synovial fluid: potential confusion with calcium pyrophosphate dihydrate and apatite crystals.

Silicon-containing particles were identified by transmission electron microscopy (TEM) in thin sections of two synovial fluids, which also contained calcium pyrophosphate dihydrate (CPPD) crystals, aspirated during acute attacks of pseudogout. Such particles, which are interpreted as probably being artefacts from glassware, were electron dense and similar in appearance to some CPPD or hydroxyapatite crystals.

Aged↗
PubMed2006

Comparison of characteristics of patients with and without calcium pyrophosphate dihydrate crystal deposition disease who underwent total knee replacement surgery for osteoarthritis.

OBJECTIVE: To compare characteristics of patients with severe osteoarthritis with and without calcium pyrophosphate dihydrate (CPPD) crystal deposition disease. STUDY METHODS: Patients undergoing total knee replacement surgery participated in this study and completed questionnaires. Radiographs of the index knee (extended anteroposterior, lateral and skyline) were reviewed for the presence of chondrocalcinosis. Synovial fluids were obtained during surgery and analyzed under compensated polarized light microscopy. RESULTS: The presence of CPPD crystals was identified in 52.9% of 102 patients. The use of both radiographs and synovial fluid analysis increased the identification of crystals. There was no difference in the following characteristics of the patients with and without CPPD crystals: age of pain onset, gender, difficulty in performing daily functions (including cooking, standing up from chairs, using restroom, going upstairs, and going shopping), history of previous joint inflammation, use of walking aids, and number and types of medications ever used. CPPD patients underwent knee arthroplasty at older age compared to non-CPPD patients (70.3+/-6.37 and 67.5+/-7.15 years old, respectively) (P = 0.037). All but one CPPD patients were unaware of the presence of crystals. CONCLUSION: High prevalence of CPPD crystals was found in patients undergoing total knee replacement surgery. All but one CPPD patients were unaware of calcium deposition in the index joints. Patients with these crystals experienced similar difficulties in performing daily activities and received similar treatment to patients without CPPD crystals. CPPD patients did not undergo knee arthroplasty at earlier age than non-CPPD patients.

Aged↗
PubMed1987

Sequential study of pleural peritoneal and blood cells in acute pleurisy induced by calcium pyrophosphate in the rat.

We studied the sequential cellular events that occur during nonspecific pleurisy induced by a nondiffusible, nonantigenic and endotoxin-free irritant, calcium pyrophosphate (CaPP). The study was conducted over 10 days and concerned not only the pleural cavity but also the peritoneal cavity and the blood. After injection of CaPP, the first cellular event in the pleural space was a "leukocyte disappearance reaction," followed by an important increase in the polymorphonuclear leukocytes (PMN) and then by an increase in the macrophages. This phase is also characterized by the appearance of submesothelial nodules composed of macrophages and numerous polymorphonuclear cells. All the cell populations returned to their normal value on day 10, although granulomatous submesothelial nodules were present. In the blood, the principal observation was an increased PMN count associated with a decreased lymphocyte count at 4 h. In the peritoneal cavity, it was remarkable that, although functional modifications have been reported in the same model, the different leukocyte populations did not vary during the reaction.

Animals↗
PubMed2006

"Crystal clear"-sonographic assessment of gout and calcium pyrophosphate deposition disease.

OBJECTIVES: To date, high-resolution ultrasound (US) has not been fully exploited in the field of crystalline arthropathy. Both gout and calcium pyrophosphate deposition (CPPD) disease are significant diseases within the purview of the rheumatologist. The aim of this pictorial review was to present the principal findings in patients with crystal deposition in gout and CPPD. METHODS: US pictures were obtained from 60 consecutive patients, 34 with CPPD disease and 26 with gout, whose diagnosis was confirmed by synovial fluid analysis. The US examinations were performed using the following US systems: Diasus (Dynamic Imaging, Livingstone, UK) and Logiq 9 (General Electric Medical Systems, Milwaukee, WI). RESULTS: Pictorial evidence of the principal US findings in gout includes monosodium urate (MSU) deposition on the surface of articular cartilage, various patterns within synovial fluid ranging from completely anechoic fluid to collections filled with aggregates of variable shape and echogenicity, microdeposition within tendons, and tophus formation. In CPPD, the hallmark US features include crystal deposition within articular cartilage, calcification of fibrocartilage, together with focal crystal deposition within tendons. CONCLUSION: US is an impressive imaging modality in crystalline arthropathy. The anatomical location of the crystal deposits, clearly depictable by US, allows differentiation between MSU and CPPD aggregates.

Arthritis, Gouty↗
PubMed1988

Calcium pyrophosphate crystal deposition in hyaline cartilage. Ultrastructural analysis and implications for pathogenesis.

Using transmission electron microscopy, selected area electron diffraction, and micro x-ray diffraction techniques, we studied calcium pyrophosphate dihydrate (CPPD) deposits from 23 patients with chondrocalcinosis affecting the femoral head to delineate the cellular and matrix environment in which CPPD crystals form, to determine the sequence of crystal deposition, and to address the question of coexistent calcium apatite crystal deposition. We found 2 types of CPPD crystal deposits with few transitional forms. First, small collections of crystals were seen at the border of the territorial matrix at the articular and subarticular poles of the chondron. CPPD crystal deposits were unassociated with collagen or matrix vesicles. Second, and more frequently, large collections of randomly arranged crystals (agglomerates) were observed, the smallest replacing the chondrocyte and adjacent pericellular matrix. Chondrocytes adjacent to crystal deposits were intact. Coexistent apatite crystal deposition was demonstrated in only 2 of 23 cartilages ultrastructurally examined, providing evidence that mixed crystal deposits are possible but not common in CPPD crystal arthropathy.

Aged↗