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Results for “Calcium Pyrophosphate”

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PubMed1992

Extraction of calcium containing crystals from synovial fluids and articular cartilage.

A protocol for extracting minerals from biological tissues and fluids has been developed. Synovial fluid (SF) and articular cartilage samples were treated with papain and sodium hypochlorite to extract and concentrate calcium containing crystals. The method was validated by testing the ability to reextract synthetic calcium pyrophosphate dihydrate and calcium hydroxyapatite crystals added to SF in an unchanged form. The extracted crystals were analyzed by infrared spectroscopy and X-ray powder diffraction. The concentration of both calcium pyrophosphate dihydrate and hydroxyapatite crystals in SF was found to be higher than published figures.

Calcium↗

PubMed2000

Gout and other crystal-associated arthropathies.

Intra-articular crystals (monosodium urate monohydrate, calcium pyrophosphate dihydrate, basic calcium phosphates) can cause acute and chronic inflammation and joint damage. Identification of the crystals by polarized microscopy is the key step in diagnosis but improved reliability of synovial examination is required. Treatment of disorders associated with gout or calcium pyrophosphate deposition may reduce non-joint morbidity and assist treatment of the arthritis. Various forms of anti-inflammatory therapy work for acute crystal-induced arthritis; prompt commencement is usually more important than which option is used. In gout, recurrent attacks are usual, but hypouricaemic therapy is almost never urgent, is life-long, and is too often negated by poor compliance. In most patients, allopurinol or any of the potent uricosuric drugs will allow maintenance of normouricaemia but renal failure, renal calculi, transplantation, and allopurinol allergy narrow the options and complicate management.

Calcium↗

PubMed2005

Extracellular matrix changes regulate calcium crystal formation in articular cartilage.

PURPOSE OF REVIEW: The pathologic matrix mineralization seen in calcium pyrophosphate dihydrate and basic calcium phosphate deposition diseases identifies a subset of osteoarthritis patients with an unusual joint distribution and rapid progression of disease. Several factors contribute to pathologic matrix mineralization, including changes in the extracellular matrix of articular cartilage. The factors contributing to extracellular matrix changes that promote crystal formation are important and not well understood. Better characterization of these factors will enhance the understanding of the pathogenesis of pathologic matrix mineralization and may identify potential targets for novel therapeutic interventions. RECENT FINDINGS: Histologic studies of cartilage from patients affected by calcium crystal arthritis show changes in the pericellular matrix of articular chondrocytes. The amounts and types of collagens, proteoglycans, and calcium-binding proteins are altered. The mechanisms by which these changes occur remain poorly understood. Recent work, however, has implicated alterations in the chondrocyte phenotype and post-translational matrix-modulating enzymes such as the transglutaminases. SUMMARY: Changes in extracellular matrix are associated with the pathologic matrix mineralization seen in calcium pyrophosphate dihydrate and basic calcium phosphate crystal deposition diseases. The literature on growth plate cartilage provides observations and mechanisms through which extracellular matrix contributes to normal matrix mineralization, and has served as a model on which to base studies in articular cartilage. More studies are warranted to enhance the understanding of how changes in extracellular matrix contribute to crystal deposition diseases.

Calcium Phosphates↗

PubMed1975

Calcium pyrophosphate-induced pleurisy in rats: a new model of acute inflammation.

A model is described of acute inflammation in the pleural cavity of rats using calcium pyrophosphate as the irritant. This model would seem to simulate the pseudogout syndrome. It has been shown to be acute in onset, dominated by polymorphonuclear cells, complement independent. The advantage of the model is that volume of exudate, numbers and types of cells may be quantitated. Prostaglandins and cyclic AMP have been measured in the migrating cells. The significance of these findings has been discussed.

Animals↗

PubMed1981

A three-year clinical caries evaluation of the effect of a sodium fluoride-silica abrasive dentifrice.

This study was conducted to determine if the anticaries effectiveness of a 0.243% sodium fluoride-silica abrasive dentifrice is superior to a 0.4% stannous fluoride-calcium pyrophosphate dentifrice. A nonfluoride, calcium pyrophosphate abrasive placebo dentifrice was also included at one-third the sample size of the active treatment groups to estimate the level of efficacy of the sodium fluoride dentifrice. A total of 3,093 schoolchildren were randomly assigned at a ratio of 3:3:1 to the sodium fluoride dentifrice, the stannous fluoride dentifrice, or the placebo dentifrice, respectively. Caries examinations were made by the same examiner initially and after one, two, and three years of ad libitum product usage. After three years, the results showed that the group using the sodium fluoride dentifrice had significantly fewer DMF teeth and DMF surfaces increments than the group using the stannous fluoride dentifrice. The percent reductions for DMF teeth and DMF surfaces were 24.2% and 22.6%, respectively. Both groups using fluoride dentifrices also had significantly fewer DMF teeth and DMF surfaces increments than the group using the placebo dentifrice.

Adolescent↗

PubMed2004

In vitro models of calcium crystal formation.

PURPOSE OF REVIEW: Calcium pyrophosphate dihydrate crystals are common components of synovial fluids from degenerated joints and often accompany unusually severe cartilage destruction. Progress in understanding why and how calcium pyrophosphate dihydrate crystals form in articular cartilage has been hampered by the scarcity of good models in which to study this phenomenon. RECENT FINDINGS: In this review, the author discusses various models of calcium pyrophosphate dihydrate crystal formation from early work with solutions and gels to more recent models using cells, tissues, and cell fractions. Each of these systems has advantages and disadvantages. SUMMARY: Current models of calcium pyrophosphate dihydrate crystal formation are less than ideal for studying the major factors involved in calcium pyrophosphate dihydrate crystal formation. Borrowing from the transplantation literature, solid matrices that support cell growth and allow for easy manipulation of matrix components hold some promise for better models in the future.

Animals↗

PubMed1993

Scanning electron microscopic study of the effect of citrate and pyrophosphate on calcium oxalate crystal morphology.

The effects of citrate and pyrophosphate on the morphology of calcium oxalate monohydrate crystals formed in a supersaturated calcium oxalate solution were examined by scanning electron microscopy. Within the normal range of urinary concentrations, citrate and pyrophosphate affected the morphology of the crystals. The length/width ratio of the crystals decreased at higher concentrations of citrate and pyrophosphate. Citrate seems to have a dual mechanism of inhibition of crystal growth (binding to the crystal surfaces) and of complexation (with calcium in the solution). Pyrophosphate is believed to bind preferentially to calcium in the solid phase rather than in the solution phase, as it affected crystal morphology at very low concentrations and was detected on the crystals by X-ray microanalysis. Pyrophosphate seems to bind to the monohydrate but not to the dihydrate.

Calcium Oxalate↗

PubMed1980

Subcutaneous crystal deposition in pseudogout.

Aspiration of inflamed periarticular tissues in seven patients suspected of having gout on clinical examination revealed positively birefringent calcium pyrophosphate crystals. The identification of calcium pyrophosphate crystals within articular structures and in the surrounding soft tissues and radiologic findings of chondrocalcinosis, in the absence of identifiable uric acid crystals, emphasize the importance of crystal identification in all cases of probable gout and stress the diagnostic role of soft-tissue aspiration in cases of soft-tissue inflammation, especially when arthrocentesis is unsuccessful.

Adult↗

PubMed1996

Calcium crystal-associated diseases.

The significance of calcium-containing crystals is unknown. Circumstantial evidence suggests that crystals are associated with more severe arthritis. Addition of calcium pyrophosphate dihydrate crystals to a lapine meniscectomy model of osteoarthritis resulted in greater damage to cartilage compared with meniscectomy alone. Elimination of calcium pyrophosphate dihydrate crystals may occur extracellularly by enzymatic degradation. Spermine and spermidine both enhance the degradative activity of alkaline phosphatase on crystals. In familial calcium pyrophosphate dihydrate crystal deposition disease, genetic heterogeneity is likely because one family demonstrated a linkage to chromosome 8q, whereas another did not. Tumoral deposition of calcium pyrophosphate dihydrate crystals may occur in single locations without radiographic chondrocalcinosis in other joints. Hydroxyapatite crystals are found in the ligamenta flava from surgical specimens but not as tumoral depositions. Magnesium whitlockite crystals have been found not only in osteoarthritic articular cartilage but also in normal cartilage, suggesting that these crystals may be nonpathologic in at least some cases.

Calcium↗

PubMed2000

ATP release by mechanically loaded porcine chondrons in pellet culture.

OBJECTIVE: To determine whether ATP is released from chondrocytes during mechanical stimulation and whether degradation of ATP generates inorganic pyrophosphate in chondron pellet cultures. METHODS: Chondron pellets were formed from 1.6 x 10(6) cells that had been enzymatically isolated from porcine articular cartilage. ATP was measured in media from cultures at rest and during fluid movement and cyclic compression. ATP hydrolysis was examined by high-performance liquid chromatography following the addition of gamma32P-ATP to resting cultures. RESULTS: Pellet cultures at rest maintained a steady-state concentration of 2-4 nM ATP in 2 ml of medium. The ATP concentration increased 5-12-fold with cyclic compression (7.5 and 15 kPa at 0.5 Hz), then decreased to preloading levels within 60 minutes despite continued loading. A subsequent increase in pressure stimulated a further increase in ATP release, suggesting that chondrocytes desensitize to load. Cell viability was similar for pellets at rest and up to 24 hours after compression. ATP released in response to mechanical stimulation was inhibited 50% by 0.5 mM octanol, suggesting a regulated mechanism for ATP release. Exogenous ATP was rapidly hydrolyzed to pyrophosphate in resting cultures. CONCLUSION: The occurrence of basal levels of extracellular ATP in the presence of pyrophosphohydrolase activity indicates that ATP was continuously released by chondrocytes at rest. Considering that chondrocytes express purinoceptors that respond to ATP, we suggest a role for ATP in extracellular signaling by chondrocytes in response to mechanical load. ATP released by chondrocytes in response to mechanical load is a likely source of pyrophosphate in calcium pyrophosphate dihydrate crystal deposition diseases.

Adenosine Triphosphate↗

PubMed1992

Permanent stained preparations of synovial fluid for detection of calcium compounds using alizarin red S.

Permanent preparations of air dried synovial fluids were prepared by staining calcium compounds with alizarin red S stain; each slide was coverslipped with Permount. Variables studied were: (a) concentration of the solution of alizarin red S, (b) pH of staining solution, (c) time of incubation in staining solution and aqueous and ethanolic content of staining solution. The staining effect of each solution was tested on calcium pyrophosphate dihydrate, calcium oxalate, apatite and monosodium urate (MSU). Of all the solutions, best results were obtained with 0.25% alizarin red S in 50% ethanol at pH 7.0 for 30 min. With this solution, the calcium-containing compounds were well stained. MSU did not stain and still preserved negative birefringence on polarization. Fixation of smears with ethanol served a double purpose: It fixed the slides without dissolving or removing MSU or the calcium compounds, yet it did dissolve five corticosteroids commonly used for intra-articular injection which may interfere with interpretation of compensated polarized light microscopy of synovial fluids.

Anthraquinones↗

PubMed1993

Accidental superphosphate fertilizer poisoning in pregnant ewes.

Consumption of superphosphate fertilizer by 200 pregnant ewes resulted in signs of toxicosis in 41 ewes, 14 of which died. Predominant clinical signs were marked teeth grinding, voluminous diarrhea, CNS depression, apparent blindness, and a stiff-legged atactic gait. Biochemical abnormalities were hypocalcemia, hypoglycemia, and a high anion gap. The primary toxic principal in superphosphate fertilizers is the fluorine contaminant; however, calcium pyrophosphate and calcium orthophosphate also contribute to toxicosis, which results in acute proximal renal tubular necrosis. Voluntary consumption of superphosphate fertilizer in well-fed livestock is not expected, and was believed to be related to the lack of availability of salt.

Animals↗

PubMed1995

Adsorption of 5'-AMP and catalytic synthesis of 5'-ADP onto phosphate surfaces: correlation to solid matrix structures.

A non-enzymatic formation of 5'-ADP starting from phosphorylation of 5'-AMP in the presence of either calcium phosphate or calcium pyrophosphate precipitates is reported. This reaction is taken as a model for the study of heterogeneous catalysis of transphosphorylation in prebiotic conditions. Experiments were performed in completely aqueous media and in media containing dimethyl sulfoxide (Me2SO), to simulate periods of dehydration in primitive aquatic environments. It has been observed that the nucleotide is adsorbed onto both calcium phosphate and calcium pyrophosphate in accordance with Langmuir isotherms. Adsorptive capacity and affinity of the precipitates for nucleotide are changed by the presence of Me2SO, suggesting that the interaction between biomonomers and surfaces can be modulated by the degree of hydration of the anionic components of these compounds. In completely aqueous environments, formation of 5'-ADP from 5'-AMP adsorbed on precipitates of calcium phosphate and calcium pyrophosphate is very small. However, in the presence of 60% Me2SO this synthesis increases by factors of 3 and 6 for surfaces of calcium phosphate and calcium pyrophosphate, respectively, and follows first-order kinetics. Determinations of free energy changes show that phosphorylation of 5'-AMP adsorbed to these precipitates is thermodynamically favorable. Depending on the precipitation time of the samples and the composition of the medium, structural analysis of these precipitates by electron and X-ray diffraction shows changes in their cristallinity grade. It is proposed that these changes are responsible for the modulation of the quantity of adsorbed nucleotides to the surface of solid matrices as well as the catalytic activity of the precipitates.

Adenosine Diphosphate↗

PubMed1991

Crystal arthritis: a clinician's view.

Arthritis, which can be acute, chronic or asymptomatic, is caused by a variety of crystal deposition in joints. The three main types of crystal arthritis are monosodium urate (gout), calcium pyrophosphate dihydrate, and calcium phosphate (usually hydroxyapatite). A clinical approach to diagnosis and management.

Adrenal Cortex Hormones↗

PubMed1994

[Mechanism of crystal deposition in the joints].

The mechanism of crystal deposition in joints varies with the chemical nature of the crystal. Crystallisation of monosodium urate, characteristic of gout, requires a neutral pH and supersatured tissues, which is the basis for the clinical definition of the upper limit of normal blood uric acid level. The appearance of crystals also is dependent on time since crystallisation of monosodium urate is very slow. Inhibitory or promoting factors could intervene and explain rare cases of gout without hyperuricemia or the rapid crystallisation which seems to characterise some types of drug-induced gout. Crystal deposits of calcium pyrophosphate dihydrate form mainly in the cartilage where they seem favoured by ageing or by trauma, which could deplete cartilage of crystallisation inhibitors, notably proteoglycans. High pyrophosphate levels within cartilage also play an important role. The appearance of these pyrophosphates in the interstitial cartilagenous medium would be in large part due to the activity of an ectoenzyme, nucleoside triphosphate pyrophosphatase; increased activity of this ectoenzyme could be responsible for some chondrocalcinosis. Chronic hypercalcaemia can also be involved in the pathogenesis of cartilage deposition of calcium pyrophosphate dihydrate by raising the calcium-pyrophosphate product, or by decreasing the activity of alkaline phosphatase, an enzyme responsible for breakdown of extracellular pyrophosphates. The pathophysiology of calcium phosphate deposits is poorly understood. For some authors, these deposits occur within matrix vesicles, but for others, within collagen fibres. Increase in the calcium-phosphate product can also be a cause, for example, during renal osteodystrophy or vitamin D intoxication.(ABSTRACT TRUNCATED AT 250 WORDS)

Arthritis↗

PubMed1994

Crystals and arthritis.

Monosodium urate, calcium pyrophosphate dihydrate, and basic calcium phosphate (carbonate-substituted hydroxyapatite and octacalcium phosphate) crystal aggregates are associated with gout, pseudogout, and cartilage degeneration (osteoarthritis, Milwaukee Shoulder/Knee Syndrome), respectively. Hyperuricemia is a frequent but nonspecific and inconstant feature of gout just as an elevated synovial fluid inorganic pyrophosphate level is an inconstant feature of pseudogout. Monosodium urate, calcium pyrophosphate dihydrate, or basic calcium phosphate crystals can cause acute inflammation associated with phagocytosis by neutrophilic leukocytes. Each induces neutral protease synthesis and secretion and arachidonic acid metabolism by synoviocytes and macrophages in a dose-dependent fashion, postulated to produce the damage to bone, cartilage, and other joint tissues that is perceived clinically as tophaceous destruction or degenerative joint disease. Crystals containing calcium are potent mitogens. All three types of crystals are more common in older persons and will attract additional attention as the mean age of our population increases. Gout is perhaps the most treatable disease in medicine, although mistakes in diagnosis and in choice of appropriate therapy are very common. Acute pseudogout and acute calcific periarthritis are readily treated medically, but the chronic effects of crystals containing calcium are not. New approaches using drugs derived from scientific study of the biologic effects of these crystals may become useful therapeutically.

Arthritis↗

PubMed1984

Cartilage calcification: normal and aberrant.

Hydroxyapatite crystal deposition occurs physiologically in cartilage as a prelude to bone formation via endochondral ossification. Both extracellular molecules and organelles, and the chondrocytes themselves control the initial formation of hydroxyapatite, as well as the growth and orientation of the hydroxyapatite crystals. In this study pathologic calcium containing deposits from 48 patients (27 hydroxyapatite and 21 calcium pyrophosphate dihydrate) were subjected to crystallographic, histologic (light microscopy, scanning electron microscopy, transmission electron microscopy) and chemical analyses and compared to normal controls. It is suggested that both hydroxyapatite and calcium pyrophosphate dihydrate deposition involve elevations in ionic concentrations, exposure of mineral nucleators, and removal of mineral inhibitors. Peculiar to the matrices of pathologic deposits of hydroxyapatite are elevated concentrations of calcium acidic phospholipid phosphate complexes and lower concentrations of hexosamine while collagen (hydroxyprolin) and total lipid contents are not altered. Matrices of deposits of calcium pyrophosphate dihydrate were similar biochemically except that calcium acidic phospholipid phosphate complexes concentrations were not elevated.

Calcification, Physiologic↗

PubMed1975

A clinical evaluation of a sodium fluoride dentifrice.

A double-blind study to determine the anticaries efficacy of a neutral pH dentifrice containing sodium fluoride and a high Beta-phase calcium pyrophosphate was conducted among elementary school children in Kansas City, Missouri. A sample of 567 children ages 8-13 were recruited and randomly assigned to test and control groups: the test group received a sodium fluoride high Beta-phase calcium pyrophosphate dentifrice, and the control group received a calcium pyrophosphate dentifrice without the active ingredient. The sodium fluoride dentifrice contained fluoride at the level of 1000 ppm. Caried examinations were conducted at initiation, after 12 months, and again after 24 months at the study's termination. All examinations (clinical and radiographic) were performed by the same investigator. At 12 months the sodium fluoride dentifrice demonstrated a caries reduction of 24.1% (DMFS). At 24 months the reduction demonstrated was 30.1% (DMFS); this reduction is significant at alpha = 0.05.

Adolescent↗