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PubMed1987

Monosodium urate and calcium pyrophosphate crystals differentially activate the excitation-response coupling sequence of human neutrophils.

The activation patterns of human neutrophils elicited by unopsonized monosodium urate and calcium pyrophosphate dihydrate crystals were investigated. The parameters chosen, the mobilization of calcium and the synthesis of leukotrienes, are generally accepted to be relevant to the activation of the cells and their pathophysiological roles. Both particles were found to elicit increases in cytoplasmic free calcium and leukotriene synthesis. However, the rank order of potency of these two stimuli was found to be sharply dependent on the test chosen. Monosodium urate crystals were significantly more effective than calcium pyrophosphate dihydrate crystals in terms of calcium mobilization, while the latter are more potent at inducing leukotriene synthesis. These results demonstrate that these two phagocytic particles which are related to separate inflammatory joint diseases differentially activate the excitation-response coupling sequence of human neutrophils.

Arachidonate 5-Lipoxygenase↗

PubMed2006

Preparation and characterization of RF magnetron sputtered calcium pyrophosphate coatings.

CaP ceramic has been widely used as coating on metals in orthopedics and oral dentistry. Variations in CaP composition can lead to different dissolution/precipitation behavior and may also affect the bone response. In the present study calcium pyrophosphate and hydroxylapatite coatings were successfully prepared by RF magnetron sputtering deposition. The phase composition, morphological properties, and the dissolution in SBF were characterized by using XRD, FTIR, EDS, SEM, and spectrophotometry. The results showed that all the sputtered coatings were amorphous and changed into a crystal structure after IR-radiation. The temperature for the crystallization of the amorphous coatings is lower for the hydroxylapatite coating (550 degrees C), compared to the calcium pyrophosphate coating (650 degrees C). All sputtered amorphous coatings were instable in SBF and dissolved partially within 4 wks of incubation. The heat-treated coatings appeared to be stable after incubation. These results showed that magnetron sputtering of calcium pyrophosphate coating is a promising method for forming a biocompatible ceramic coating.

Calcium Pyrophosphate↗

PubMed1991

Deposition of calcium pyrophosphate dihydrate crystals in a soft tissue chondroma.

Calcium pyrophosphate dihydrate (CPPD) crystal deposits were found in an extraarticular chondroma of the soft parts overlying the distal phalanx of the right middle finger. The lesion appeared to arise from the flexor tenosynovium. The pathogenesis of soft tissue chondroma and the relation of cartilage metaplasia to the process of CPPD crystal deposition were investigated.

Aged↗

PubMed1997

Phosphocitrate inhibits a basic calcium phosphate and calcium pyrophosphate dihydrate crystal-induced mitogen-activated protein kinase cascade signal transduction pathway.

Calcium deposition diseases caused by calcium pyrophosphate dihydrate (CPPD) and basic calcium phosphate (BCP) crystals are a significant source of morbidity in the elderly. We have shown previously that both types of crystals can induce mitogenesis, as well as metalloproteinase synthesis and secretion by fibroblasts and chondrocytes. These responses may promote degradation of articular tissues. We have also shown previously that both CPPD and BCP crystals activate expression of the c-fos and c-jun proto-oncogenes. Phosphocitrate (PC) can specifically block mitogenesis and proto-oncogene expression induced by either BCP or CPPD crystals in 3T3 cells and human fibroblasts, suggesting that PC may be an effective therapy for calcium deposition diseases. To understand how PC inhibits BCP and CPPD-mediated cellular effects, we have investigated the mechanism by which BCP and CPPD transduce signals to the nucleus. Here we demonstrate that BCP and CPPD crystals activate a protein kinase signal transduction pathway involving p42 and p44 mitogen-activated protein (MAP) kinases (ERK 2 and ERK 1). BCP and CPPD also cause phosphorylation of a nuclear transcription factor, cyclic AMP response element-binding protein (CREB), on serine 133, a residue essential for CREB's ability to transactivate. Treatment of cells with PC at concentrations of 10(-3) to 10(-5) M blocked both the activation of p42/p44 MAP kinases, and CREB serine 133 phosphorylation, in a dose-dependent fashion. At 10(-3) M, a PC analogue, n-sulfo-2-aminotricarballylate and citrate also modulate this signal transduction pathway. Inhibition by PC is specific for BCP- and CPPD-mediated signaling, since all three compounds had no effect on serum-induced p42/P44 or interleukin-1beta induced p38 MAP kinase activities. Treatment of cells with an inhibitor of MEK1, an upstream activator of MAPKs, significantly inhibited crystal-induced cell proliferation, suggesting that the MAPK pathway is a significant mediator of crystal-induced signals.

Calcium Phosphates↗

PubMed1985

[A clinical study of calcium pyrophosphate dihydrate crystal deposition disease].

Clinical features of calcium pyrophosphate dihydrate crystal deposition disease (CPPD c.d.d.) were studied and the following results were obtained. The prevalence of CPPD c.d.d. was 9.7% in 300 persons aged 50 or older, who stayed or worked at an old-age home. The most common type of CPPD c.d.d. was the asymptomatic type. Comparative studies between the patients with CPPD c.d.d. and subjects without it revealed that scoliosis of the lumbar spine, osteoarthritis-like changes of the knee, subchondral bone cyst and patella wrapped around the femur were statistically more frequent in the former. The clinical study of 50 patients with CPPD c.d.d. revealed calcification not only in the articular cartilage but also in periarticular tissues and ligamentum flavum. The histological study demonstrated frequent destructive changes of the tissues around the site of CPPD crystal deposition. Formation of CPPD crystals appeared to be initiated by degenerating chondrocytes and metaplastic chondrocytes.

Age Factors↗

PubMed1996

Mixed monosodium urate and calcium pyrophosphate crystal-induced arthropathy. A review of seventeen cases.

Among 4620 synovial fluid specimens examined in our laboratory from 1989 through 1992, 18.3% contained crystals (calcium pyrophosphate dihydrate, 55.7%; monosodium urate, 42%). Both calcium pyrophosphate dihydrate and monosodium urate crystals were found in 17 patients, usually in specimens obtained from the knee. Only five of these 17 patients had a known history of gout. Among the patients with a mixed crystal composition, the females had a higher mean age (78.5 years) than the males (53.2 years), in keeping with the fact that gout is exceedingly rare in premenopausal women. The two youngest men (40 and 45 years) had a history of meniscectomy, which is a known risk factor for early chondrocalcinosis.

Adult↗

PubMedDate not supplied

[Suture granuloma with calcium pyrophosphate deposits].

In the report two foreign body granulomas, one observed in the fibrous periarticular tissue and the other one in tendo achilles with depositions of crystals inside the granulomas are described. Polarisation microscopy exhibited birefringent crystals which stained black with the van Kossa reaction. The scanning electron microscopic appearance was that of calcium-pyrophosphate-dihydrate when compared with crystals of menisceal tissue in "chondrocalcinosis". The structure of the crystals was different from those that can be observed in calcifying tendinitis or in calcified scars. By X-ray microanalysis nearly identical peaks for calcium and phosphorus were measured, indicating the atomic composition of calcium-pyrophosphate-dihydrate. For the crystalline deposits were restricted to an acellular tissue between the foreign body material it is concluded that necroses in the fibrous periarticular tissues or tendons may be prone for deposition of calcium-pyrophosphate.

Achilles Tendon↗

PubMed1975

Factors affecting the solubility of calcium pyrophosphate dihydrate crystals.

The solubility of triclinic calcium pyrophosphate dihydrate (CPPD) crystals was measured under varying conditions using 45Ca-labeled crystals, expressing solubility as micromoles per liter of 45Ca in solution. In a 0.1-M Tris-HC1 buffer pH 7.4, the solubility of accurately sized CPPD crystals (37-20mum) was 60muM with maximal solubility being attained after about 8 h incubation at 37degreeC. Reduction in crystal size, decrease in pH, increase in ionic strength, Mg++, citrate, and albumin all increased solubility. The most marked effects on solubility occurred when changing the calcium concentration or by enzymatic hydrolysis of inoganic pyrophosphate to orthophosphate. It was found that decreasing the ionized calcium level below 5 mg/100 ml resulted in a progressive enhancement of solubility. The observed solubility-enhancing effects of albumin could be explained solely on its calcium-binding ability and thereby, altered ionized calcium level. Diffusible calcium in synovial fluid was only 40% of the total calcium concentration, which means most joint fluids are normally near the critical concentration of 5 mg/100 ml of ionized calcium, below which solubility is enhanced. During surgery, especially parathyroidectomy, calcium levels fall, favoring dissolution of CPPD crystals. We speculate that the slight decrease in crystal size during dissolution frees them from their cartilaginous mold, resulting in a dose-dependent inflammatory reaction as they are "shed" into the joint space. Crystal shedding may be reinforced by the modest fall in joint fluid pH accompanying the inflammatory response.

Arthritis, Rheumatoid↗

PubMed1996

Periodontoid calcium pyrophosphate dihydrate deposition disease: "pseudogout" mass lesions of the craniocervical junction.

Between 1984 and 1996, seven patients with symptomatic masses located posterior to the odontoid process and containing calcium pyrophosphate dihydrate crystals were evaluated by the senior author (A.H.M). All patients presented with distal paresthesias and myelopathy and underwent transoral-transpharyngeal resection of the anterior arch of C-I, the odontoid process, and the compressing mass. Histological examination revealed the characteristic changes of calcium pyrophosphate dihydrate (CPPD) deposition disease, with nodular deposits of birefringent rhomboid crystals. On magnetic resonance imaging, the masses appeared predominantly isointense with neural tissue on T1-weighted images and iso-to hyperintense on T2-weighted images. On computerized tomography scans, small area of calcifications within the masses were apparent in all cases. All patients improved postoperatively, with six of seven patients requiring posterior fixation for instability as a second procedure. Calcium pyrophosphate dihydrate deposition causing periodontoid mass lesions is a distinct clinical disease entity that probably is underdiagnosed. In the authors' l opinion, the diagnosis can often be established preoperatively by the distinctive neuroradiological appearance of the masses. Therefore, CPPD deposition disease should be considered in the differential diagnosis of masses of the craniocervical junction, because it is amenable to early surgical intervention. The consulting neuropathologist should be made aware of this diagnostic possibility at the time of surgery.

Aged↗

PubMed1976

Calcium pyrophosphate. Histological characterization of crystals in pseudogout.

Deposits taken from an acetabulum and the head of a femur and known to contain crystals of calcium pyrophosphate were examined by selected histological methods for calcium after the application of a variety of solvents. Treatment with 10% ferric chloride removed all calcium salts tested, except a birefringent crystalline component in the pyrophosphate deposits. This corresponds to the previous optical and morphological descriptions of calcium pyrophosphate as found in synovial fluids. Calcium pyrophosphate stains consistently only by the fluorescent morin method.

Acetabulum↗

PubMed1992

Osteoarthritis, calcium pyrophosphate deposition disease, and osseous infection in Old World primates.

Uncertainties as to the nature and implications of osteoarthritis and calcium pyrophosphate deposition disease (CPPD) in primates were subject to critical review through examination of 153 prosimians and 1,250 Old World non-prosimian primates. Osteoarthritis, calcium pyrophosphate deposition disease, and infectious arthritis/osteomyelitis were relatively rare phenomena, affecting only 1.7% and 2.5%, respectively, of free-ranging prosimians and other Old World non-prosimian primates. Frequency of infection in Indri and Presbytis appears to reflect a unique susceptibility or exposure. Papio may have a unique predisposition to CPPD. The dichotomy (frequency and joint distribution) between free-ranging and artificially restrained animals suggests caution in interpretation of osteoarthritis or CPPD in non-free-ranging animals.

Animals↗

PubMed1991

Histochemical localization of calcium with potassium pyroantimonate in the articular tissues in calcium pyrophosphate dihydrate crystal deposition disease.

The ultrastructural localization of calcium in the articular cartilage, meniscus, and synovium of patients with calcium pyrophosphate dihydrate (CPPD) crystal deposition disease was examined by using potassium pyroantimonate. Focal areas with deposition of CPPD crystals in each tissue showed electron-dense precipitates of the antimony-calcium complex: (1) in the cytoplasm of hypertrophic chondrocytes around CPPD crystals, especially on the margins of intracellular lipid droplets or within electron-dense amorphous material or both; and (2) on the margins of lipid droplets and within electron-dense amorphous material in the degenerated matrix surrounding the hypertrophic chondrocytes. The slender rodlike structures consisting of electron-dense precipitates of the antimony-calcium complex, suggestive of the precursor to rodlike CPPD crystals, were also observed in the degenerated matrix. These findings suggest that the hypertrophic chondrocytes may contribute to the formation of CPPD crystals by intracellular accumulation of calcium and subsequent release of high concentration of calcium into their surrounding matrix.

Aged↗

PubMed2003

Calcium pyrophosphate dihydrate and hydroxyapatite crystal deposition in the joint: new developments relevant to the clinician.

The major types of crystals containing calcium, which causes arthropathy and periarticular disease, are calcium pyrophosphate dihydrate and basic calcium phosphates, including hydroxyapatite. Exciting advances include the identification of mutations in the gene ANKH associated with disordered inorganic pyrophosphate (PPi) transport in some kindred with familial chondrocalcinosis linked to chromosome 5p. In addition, central basic mechanisms governing cartilage calcification and their relationship to aging and osteoarthritis have now been elucidated. These include the role of plasma cell glycoprotein-1, the PPi-generating ecto-enzyme, in chondrocalcinosis and the linkage of low- grade inflammation to expression and activation of two cartilage-expressed transglutaminase isoenzymes with direct calcification-stimulating activity. This review discusses clinically pertinent new information on pathogenesis. The authors also address, in detail, current diagnostic and therapeutic issues pertaining to calcium pyrophosphate dihydrate and hydroxyapatite crystal deposition in the joint, as well as possible therapeutic directions for the future.

Calcinosis↗

PubMed1991

Effects of pyrophosphatase on dissolution of calcium pyrophosphate dihydrate crystals.

Understanding the dissolution mechanisms involved in calcium pyrophosphate dihydrate (CPPD) crystals may prove important for the development of therapy for CPPD arthropathy. We demonstrate that yeast pyrophosphatase effectively dissolved CPPD crystals in solutions. Maximum enzymatic dissolution of CPPD crystals was achieved at neutral pH and when the enzyme had access to the crystal surface. The enzymatic dissolution of CPPD crystals was highly dependent on ambient [Mg++] and [Ca++]. The stimulating effects of Mg++ on crystal dissolution in the presence of the enzyme is due to stimulation of pyrophosphatase activity and to enhanced direct release of pyrophosphate ions from the crystal surface. The inhibiting effect of Ca++ on crystal dissolution by the enzyme is mainly due to the suppression of pyrophosphatase activity.

Calcium↗

PubMed1988

Calcium pyrophosphate dihydrate crystal deposition disease in the cervical ligamentum flavum.

The authors describe three cases of cervical radiculomyelopathy caused by calcium pyrophosphate dihydrate crystal deposition disease (CPPDcdd). Radiological investigations revealed nodular calcifications, 5 to 7 mm in diameter, in the cervical ligamentum flavum compressing the spinal cord. Light microscopic, scanning electron microscopic, and x-ray diffraction studies were performed on all three surgical specimens obtained by laminectomy. In two of the cases x-ray microanalysis and transmission electron microscope studies were also performed. This study defined the presence of two patterns of crystal deposition in the ligamentum flavum. One is a nodular deposit, in which hydroxyapatite crystals are seen in the central part of the nodules, with calcium pyrophosphate dihydrate (CPPD) being distributed thinly around them. The other pattern is a linear deposit seen in multiple ligaments and composed of pure CPPD, which causes minimal thickening of the ligaments. A transitional pattern between the two types was also observed. This study revealed details of the nodular deposition of crystals in the ligamentum flavum and demonstrates that CPPDcdd and so-called "calcification of the ligamentum flavum" are the same disease: namely, CPPDcdd. Hydroxyapatite is assumed to have been transformed from CPPD.

Aged↗

PubMed1984

Calcium pyrophosphate deposition in nonhuman primates.

Naturally occurring deposition of calcium pyrophosphate has been identified in six rhesus monkeys following acute episodes of trauma and various septicemias. Scanning electron microscopy with energy-dispersive X-ray analytical system and single crystal electron diffraction studies were used to identify the crystals within the articular cartilage. The osteoarthritis grading system was used to determine the degree of cartilage degenerative changes.

Animals↗

PubMed1989

A histological study of calcium pyrophosphate dihydrate crystal-deposition disease.

Synovial, meniscal, articular cartilage, and other connective tissue from fifty-seven patients who had calcium pyrophosphate dihydrate crystal-deposition disease was examined by light microscopy, electron microscopy, and electron-probe microanalysis. Safranin O-positive hypertrophic chondrocytes that contained proteoglycans were observed in the tissues of each patient. Microcrystals that were suggestive of early precipitation of crystals were found in the degenerating matrix surrounding hypertrophic chondrocytes. The matrix contained electron-dense amorphous material, including proteoglycans and debris of cellular components. The microcrystals were often seen in contact with degenerating collagen fibers. There was never any histological evidence of formation of crystal in the areas that had no hypertrophic chondrocytes. Chondrocytes of this kind, surrounded by characteristic degenerating matrix, were never observed in the articular tissue from sixty-one patients who had only osteoarthritis. On the basis of our results, we speculate that electron-dense amorphous material containing proteoglycans and debris of cellular components, and the degenerating collagen fibers that were seen around the hypertrophic chondrocytes, may play important roles in the formation of calcium pyrophosphate dihydrate crystals.

Adult↗

PubMed1994

Calcium pyrophosphate dihydrate crystal deposition and other crystal deposition diseases.

Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease continues to be of intense clinical and basic science interest. Follow-up of studies of hereditary CPPD crystal deposition indicate differences from the common sporadic disease. The results of a prospective study of CPPD crystal deposition arthropathy confirm that clinical symptoms appear to be independent of radiologic progression. Novel clinical presentations include association with pregnancy and simulation of meningitis. CPPD crystal deposition pathology in synovium ultrastructurally resembles that in cartilage. Factors such as the presence of ATP can induce experimental calcifications in tissue culture that resemble CPPD crystal deposition. Interleukin-8 and tyrosine phosphorylation of neutrophil protons can mediate CPPD crystal deposition-associated inflammation. The control of crystal function and dissolution recently has been the subject of many general reviews. The theory outlined in these papers is important for understanding CPPD crystal deposition and basic phosphate crystal formation and dissolution.

Arthritis, Gouty↗