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At least 181 records · Page 10Linked to original sources
PubMed1977

A mechanism of action for non-steroidal anti-inflammatory agents in calcium pyrophosphate dihydrate (CPPD) crystal induced arthritis.

The acute inflammatory response to calcium pyrophosphate dihydrate crystals follows the meeting of neutrophils and crystals. The ensuing phagocytosis leads to the generation of a glycoprotein chemotactically active for neutrophils and to the release of lysosomal enzymes. Indomethacin and phenylbutazone, at therapeutic concentrations, impaired phagocytosis of the crystals and generation of chemotactic factor activity. Colchicine had no effect upon phagocytosis but significantly impaired the appearance of chemotactic factor activity.

Arthritis↗
PubMed1983

Analytical scanning and transmission electron microscopy and x-ray microdiffractometry of calcium pyrophosphate dihydrate crystal deposits in tissues.

This paper reviews current methods and applications for the detection and identification of calcium pyrophosphate dihydrate (CPPD) crystals. Methods reviewed include compensated polarized light microscopy, scanning electron microscopy, transmission electron microscopy, x-ray energy-dispersive elemental analysis, x-ray powder microdiffractometry, and selected area electron diffractometry. Although compensated polarized light microscopy is the best technique for crystal detection in pathologic fluids and tissues, because of crystal size this technique cannot discriminate easily between CPPD(M) and CPPD(T) polymorphs. To determine the presence and relative concentration of CPPD(M) and CPPD(T), x-ray or electron microdiffractometry is required. Analytical scanning and transmission electron microscopy are needed to localize crystals ultrastructurally and to determine the relationship of the crystal deposits to tissue components. The correlative application of multiple techniques on the same sample or adjacent samples provides more precise localization and identification than any single technique.

Calcium Pyrophosphate↗
PubMed1993

Calcium pyrophosphate dihydrate crystal deposition in synovium. Relationship to collagen fibers and chondrometaplasia.

OBJECTIVE: Reasons for apparent primary deposition of calcium pyrophosphate dihydrate (CPPD) crystals in some synovial membranes have not been systematically examined. We undertook the present study to investigate for and compare possible cellular and matrix factors related to the presence of these crystals in synovium and cartilage. METHODS: Ten synovial membrane specimens and 6 cartilage specimens were obtained at the time of joint surgery from 10 patients with CPPD crystal deposition disease, for light microscopic (LM) and electron microscopic (EM) studies. RESULTS: In all synovial and cartilage specimens, we found many of the small CPPD crystals aligned on or in parallel to collagen fibers, as seen by EM. In 9 of the 10 crystal-containing synovia, we found foci of chondrometaplasia adjacent to CPPD, by LM. In 7 of the synovia, including the one without LM evidence of chondrometaplasia, we observed the presence of chondrocyte-like cells by EM. We did not note any predictable relationship between the crystals and matrix vesicles, either in synovium or in cartilage. CONCLUSION: Our EM findings provide evidence of the relationship of small CPPD-like crystals, presumably early forms, to collagen fibers both in synovium and in cartilage. By LM and EM, we also demonstrate evidence of a close association between chondrometaplasia and CPPD deposits in synovium. We suggest that chondrometaplasia might be responsible for synovial CPPD formation in predisposed patients. Both the collagen fibers and chondrocyte-like cells seem to be involved in the primary formation of CPPD deposits in the synovium as well as in the cartilage.

Aged↗
PubMed2004

[Calcium pyrophosphate dihydrate deposition disease in the transverse ligament of the atlas].

Calcium pyrophosphate dihydrate (CPPD) deposits, answerable for chondrocalcinosis, are frequently observed in elderly people. Involvement of the spine is not rare. We present the case of a woman hospitalised for an acute arthritis of the right knee related to CPPD crystal deposition disease who suffered from acute neck pain. The computerised tomography showed calcified deposits in the transverse ligament of the atlas highly suggestive of CPPD deposits. This localisation seems to be very common for CPPD deposits. These CPPD crystal deposits may induce pseudo-meningitic attacks or chronic mechanical neck pain. CPPD crystal deposits in the upper cervical spine should be diagnosed when the disease is quiet, in order to avoid unnecessary investigations and therapies when an acute cervical flare occurs.

Aged↗
PubMed1992

Comparison of the acute inflammation induced by calcium pyrophosphate dihydrate, apatite and mixed crystals in the rat air pouch model of a synovial space.

Pure monoclinic or triclinic calcium pyrophosphate dihydrate (CPPD) crystals, apatite crystals or mixtures of these crystals were injected into the synovial-like space created by the rat air pouch to compare the acute inflammation induced by these crystals. Fluids were withdrawn 6 h after injection and examined for leukocyte counts, protease, prostaglandin E2 (PGE2) and tumor necrosis factor (TNF) levels. CPPD crystals (especially monoclinic CPPD) induced higher numbers of leukocytes, and more protease, PGE2 and TNF than apatite. CPPD seemed to play a predominant role in the acute inflammation induced by mixed crystals.

Animals↗
PubMed1999

Deposition of calcium pyrophosphate in tissue after revision arthroplasty of the hip.

We reviewed histologically the incidence and pathogenesis of the deposition of calcium pyrophosphate dihydrate (CPPD) crystals in the pseudocapsule, femoral and acetabular membranes and periprosthetic tissue at revision of 789 cases of failed total hip replacement. In 13, periprosthetic tissues were found to have deposits of CPPD crystals in areas of cartilaginous metaplasia; four also showed evidence of localised deposition of amyloid. None of the patients had a history of chondrocalcinosis in the hip or other joints. Cartilaginous metaplasia and other changes in periprosthetic tissues may predispose to the deposition of CPPD and associated localised amyloid.

Acetabulum↗
PubMed1988

Histologic localization of lipid in the articular tissues in calcium pyrophosphate dihydrate crystal deposition disease.

We demonstrated the histologic localization of lipid in the articular cartilage, meniscus, and synovium in calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, by staining with Sudan III. Almost all the sites of tophus-like deposits of CPPD crystals and the degenerated matrix containing low concentrations of scattered CPPD crystals stained strongly with Sudan III. Transmission electron microscopy demonstrated round or oval lipid droplets in more than half of the chondrocytes around the crystals in each of these tissues. Small lipid droplets were also seen on or around the crystals. These findings suggest that lipids are abundant at the site of CPPD crystal deposition and may be involved in CPPD crystal formation.

Aged↗
PubMed1997

Subcutaneous extensor tendon rupture associated with calcium pyrophosphate dihydrate crystal deposition disease of the wrist.

We report a patient with rupture of the ring extensor tendon associated with calcium pyrophosphate dihydrate crystal deposition disease of the wrist. Crystal deposits were noted in synovium and the triangular fibrocartilage complex. Histological examination revealed chronic synovitis with foreign body giant cell reaction to crystals. The cause of the tendon rupture was synovitis due to crystal deposition.

Aged↗
PubMed1996

Calcium pyrophosphate dihydrate deposition disease presenting as tumoral calcinosis (periarticular pseudogout).

It has been considered unusual for periarticular calcifications to consist of calcium pyrophosphate dihydrate (CPPD). We describe a patient presenting with pain and inflammation adjacent to the site of tumoral calcifications and extending to the first metatarsophalangeal joint. Aspiration of the material revealed weakly positive birefringent rhomboid shaped crystals that proved to be CPPD by atomic force microscopy. The patient had no metabolic abnormalities or radiographic chondrocalcinosis. We believe other cases similar to ours represent another clinical form of CPPD deposition disease-periarticular pseudogout.

Aged↗
PubMed1988

Ferrous [Fe++] but not ferric [Fe] ions inhibit de novo formation of calcium pyrophosphate dihydrate crystals: possible relationships to chondrocalcinosis and hemochromatosis.

To determine the physical-chemical effects of [Fe++] and [Fe ] on calcium pyrophosphate dihydrate (CPPD) crystal formation de novo, we studied CPPD crystal formation in an established model aqueous solution mixture system using physiological concentrations of Na+, Mg++, Ca++, C1-. We found that [Fe++] greater than 1 microM or [Fe ] greater than or equal to 100 microM inhibits CPPD crystal formation under conditions of [Ca++] = 1.5 mM, [Pi] = 0.1 mM, and [PPi] = 0.1 mM that simulate CPPD formation in vivo. These experiments suggest that at biological concentrations, Fe++ acts to inhibit CPPD formation but that [Fe++] depletion therapy by removal of inhibition effects may facilitate CPPD crystal formation in articular tissues.

Calcium Pyrophosphate↗
PubMed1977

Protein binding to monosodium urate monohydrate, calcium pyrophosphate dihydrate, and silicon dioxide crystals. I. Physical characteristics.

The protein adsorptive properties of monosodium urate monohydrate (MSU), silica (Si), and calcium pyrophosphate dihydrate crystals were studied by qualitative and quantitative techniques. Immunoglobulin G (IgG) was adsorbed preferentially by MSU crystals from normal human serum and demonstrated high-affinity binding isotherms when compared with several isolated proteins in solution. The physical characteristics of this reaction suggest principally an ionic mechanism, since adsorption was enhanced by decreasing pH or ionic strength. Weaker physical forces also were suggested by studies showing enhanced adsorption at lower temperatures. The following order of affinity for Si or MSU crystals was found when equal concentrations of proteins were compared: Cohn fraction II greater than lysozyme greater than beta lactoglobulin greater than bovine serum albumin greater than ovalbumin. IgG adsorption to the crystals studied may explain certain features of their biological activity. It is suggested that this phenomenon blocks the membranolytic properties of crystals and stimulates their phagocytosis through interaction with Fc receptors on the surface of the phagocytic cells.

Adsorption↗
PubMed2001

Local deposition of calcium pyrophosphate crystals in evolution of knee osteoarthritis.

The aim of the study was to investigate the frequency of development of local calcium pyrophosphate (CPPD) crystal deposition in patients with knee OA initially found negative for these crystals, as well as to discover whether prognostic indicators for this subset of patients can be found. A clinical follow-up of records of outpatients with idiopathic knee OA was established. An anteroposterior plain radiography of the knee joints was made initially and at the end of the observation period. The follow-up period needed to be more than 1 year. Patients were divided into two groups. The first included patients with knee OA who did not develop intra-articular CPPD crystal deposition during the observation period (OA group). The second included those patients whose X-rays or synovial fluid (SF) analysis in the follow-up showed these crystal deposits to be present (OA + CPPD group). There were 59 patients (42 women, 17 men) who met the selection criteria. During the observation period (8.1 + 7.4 years in the OA group, 10.4 +/- 6 years in the OA + CPPD group), intra-articular CPPD deposits were observed in 15 patients (25%): 10 on the X-rays, eight in the SF and three in both examinations. Age at diagnosis of OA and incidence of obesity were similar in both groups. There was a trend (P = 0.21) towards men developing intra-articular CPPD crystal deposits more frequently than women. OA in only one knee joint was significantly more frequent in the group with CPPD (P<0.01). Of those with CPPD deposits 40% required surgery at the end of the observation period, compared to 27.2% of those without deposits (P = 0.27). The waiting period before knee surgery was shorter in the OA + CPPD group but the difference was not statistically significant. In conclusion, local CPPD crystal deposition was observed in 25% of cases during the evolution of knee OA. No predictive factors were found. OA of the knee could, per se, favour the development of CPPD deposits. The occurrence of intra-articular CPPD deposits seemed to be related to a more rapid and severe evolution of OA of the knee.

Aged↗
PubMed1987

Characterization and membranolytic effects of triclinic calcium pyrophosphate dihydrate crystals.

The effects of incubation time and buffers of differing phosphate concentration on the ability of well characterized, synthetic triclinic calcium pyrophosphate dihydrate (CPPD) crystals to cause hemolysis of erythrocytes were determined. Maximum hemolysis was attained between 8-11 h; the percent hemolysis was 79% at a high crystal concentration of 50 mg/ml. The percent hemolysis values decreased with increasing phosphate concentration, which may have been due to adsorbed phosphate ions partially masking or protecting the erythrocyte membrane from a binding interaction with CPPD crystals. CPPD crystals possessed a significant negative surface potential, and we postulate that the CPPD crystal-membrane interaction may be mediated via an electrostatic mechanism.

Calcium Pyrophosphate↗
PubMed1984

Calcium pyrophosphate dihydrate deposits in the cervical ligamenta flava causing myeloradiculopathy.

Three cases of cervical myeloradiculopathy associated with multiple calcified nodules containing identified calcium pyrophosphate dihydrate (CPPD) crystals in the ligamenta flava are described, with a comprehensive review of the 12 cases of this entity reported to date. The disease is characterized by: 1) oval or triangular areas of radiodensity in the posterior aspect of the cervical canal as seen in the lateral x-ray films and laminograms; 2) hemispherical areas of high density located almost symmetrically in the paramedial portion of the posterior spinal canal on computerized tomography scans; and 3) CPPD crystals in the nodules. It occurs independently or in association with cervical spondylosis or ossification of the posterior longitudinal ligament.

Aged↗
PubMed2006

Subcutaneous evaluation of RF magnetron-sputtered calcium pyrophosphate and hydroxylapatite-coated Ti implants.

The in vivo behavior of infrared-heated, RF magnetron-sputtered hydroxylapatite (HA) and calcium pyrophosphate (DCPP) coated titanium discs was investigated. The discs were implanted subcutaneously in the back of six goats for 2, 4, 8 and 12 weeks. At the end of the study, coated discs were removed and examined on their physicochemical properties by X-ray diffraction (XRD) and scanning electron microscopy (SEM), including energy dispersive spectroscopy (EDS). Also, implants were prepared for light microscopical evaluation of the tissue response. The results showed that heat-treated HA coatings showed a stable behavior, i.e. no changes in the XRD pattern occurred during implantation. Also, no dissolution of the coating was observed by SEM. EDS revealed that the Ca/P ratio of the HA coatings remained stable during implantation. In contrast, heat-treated DCPP coatings showed a compositional change into apatite and tricalcium phosphate (TCP) during implantation. This was confirmed by the SEM and EDS analysis. The Ca/P ratio of the DCPP coatings changed from 0.8 to 1.52 during implantation. Finally, histology showed that both heat-treated HA and DCPP coatings showed no adverse tissue response, as characterized by the presence of thin, dense fibrous tissue capsule. Consequently, it can be concluded that 2 mum thick heat-treated, RF magnetron-sputtered HA and DCPP coatings are of sufficient thickness to withstand dissolution during 12 weeks of implantation in a subcutaneous location in goats. In addition, both coatings showed a biocompatible tissue behavior. Further, heat-treated DCPP coatings revealed a gradual compositional change into apatite and TCP.

Animals↗
PubMed1995

Evidence for a causal relationship between the structure, size, and load of calcium pyrophosphate dihydrate crystals, and attacks of pseudogout.

OBJECTIVE: To investigate any relationship between the nature, size, and numbers of synovial fluid (SF) calcium pyrophosphate dihydrate (CPPD) crystals, and attacks of pseudogout. METHODS: Knee SF was aspirated from nine selected patients, first during an attack of pseudogout (acute sample) and again later when the attack had subsided (interval sample). CPPD crystals were extracted, weighed, examined by high resolution transmission electron microscopy (HRTEM), and characterised by size and crystal habit (monoclinic or triclinic). Structural analysis was carried out by x ray powder diffraction (XRD) and the proportions of monoclinic to triclinic CPPD were estimated from densitometric measurements of selected key reflections. RESULTS: The mean crystal size, by HRTEM, indicated that the crystals in the acute sample were larger than those in the interval sample. The ratio of monoclinic to triclinic CPPD, whether estimated from their morphological appearance by HRTEM, or from XRD, was greater in the acute than in the interval sample in all nine patients. The total amount of extracted mineral varied, but in every patient the concentration of CPPD per ml of fluid, and the total mineral per joint, were greater in the acute sample than in the interval sample. CONCLUSION: In this highly selected group of patients, the large numbers of CPPD crystals associated with attacks of pseudogout included a greater proportion of monoclinic crystals, and larger crystals, than those present when inflammation had subsided. A special, phlogistic population of crystals may exist, originating in different joint tissues, or cleared in a different manner, than the more common populations of smaller crystals with a greater proportion of triclinic CPPD, seen in chronic disease.

Acute Disease↗