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PubMed1981

Comparison of phosphohydrolase activities from articular cartilage in calcium pyrophosphate deposition disease and primary osteoarthritis.

One abnormality in calcium pyrophosphate deposition disease (CPDD) which fosters consistently high synovial fluid pyrophosphate ion (PPi) and large accumulations of calcium pyrophosphate dihydrate crystals (Ca pyrophosphate) might be an aberration in chondrocytes involving elaboration of PPi and failure of its hydrolysis within cartilage matrix. Exploration of this hypothesis required further information on the phosphohydrolases in relevant human articular cartilages. Triton X-100 extracts of whole homogenized cartilage from 18 patients with primary osteoarthritis (OA), 10 patients with CPDD and secondary OA, as well as 6 "normal" subjects were partially purified by DE-52 chromatography and eluates studied for phosphohydrolase activity in a variety of substrates, inhibitors, and environmental conditions. Almost all the protein as well as crude alkaline phosphatase and pyrophosphatase activities were clustered in peaks designated I and II. Findings in CPDD cartilage not observed in OA controls were: 1) consistent alkaline phosphatase activity in the void volume of DE-52 columns, 2) high levels of 5'nucleotidase activity, 3) abundant generation of PPi by CPDD cartilage during in vitro incubation of cartilage extract fractions with ATP. This enzymatic behavior is likely to bear a regulatory relationship to PPi production by chondrocytes in CPDD.

Adenosine Triphosphate↗
PubMed1984

Calcium pyrophosphate crystal deposition. An in vitro study using a gelatin matrix model.

Deposition of crystalline triclinic (t) and monoclinic (m) calcium pyrophosphate dihydrate (CPPD) in fibrocartilage and articular cartilage is the hallmark of chondrocalcinosis. Using biologic grade gelatin to model this crystal growth process, t-CPPD, m-CPPD, amorphous calcium pyrophosphate, orthorhombic calcium pyrophosphate tetrahydrate (o-CPPT), and 3 mixed calcium/sodium pyrophosphate salts were grown at physiologic pH. Amorphous and o-CPPT appeared to be kinetic precursor crystals in the formation of t-CPPD and m-CPPD. Optimal concentration ranges for the different crystals were determined.

Calcium↗
PubMed2003

Familial calcium pyrophosphate dihydrate deposition disease and the ANKH gene.

The crystal deposition arthropathies comprise a host of disorders that may occur idiopathically or as secondary manifestations of associated diseases. Rarely, crystal deposition presents as a familial disorder. Most affected family members display radiographically detectable crystals of calcium pyrophosphate dihydrate in their joint spaces. In genetic studies of familial calcium pyrophosphate dihydrate deposition disease, a region on the short arm of chromosome 5 was found to be genetically linked to the phenotype displayed by several of these families. Among the positional candidates at this locus was ANKH, the human homolog of a gene that is responsible for the phenotype of progressive ankylosis (ank) in the mouse. ANKH codes for a transmembrane protein that appears to regulate the transport of inorganic pyrophosphate. It was analyzed as a potential positional candidate gene for calcium pyrophosphate dihydrate deposition disease, and in several unrelated families, sequence variants were identified that segregated with the calcium pyrophosphate dihydrate deposition disease phenotype among affected members. A discussion of ANKH as the familial calcium pyrophosphate dihydrate deposition disease gene is presented.

Animals↗
PubMed1986

Pyrophosphohydrolase activity and inorganic pyrophosphate content of cultured human skin fibroblasts. Elevated levels in some patients with calcium pyrophosphate dihydrate deposition disease.

In calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, metabolic abnormalities favoring extracellular inorganic pyrophosphate (PPi) accumulation have been suspected. Elevations of intracellular PPi in cultured skin fibroblasts from a single French kindred with familial CPPD deposition (19) and elevated nucleoside triphosphate pyrophosphohydrolase activity (NTPPPH), which generates PPi in extracts of CPPD crystal-containing cartilages (14) favor this suspicion. To determine whether NTPPPH activity or PPi content of cells might be a disease marker expressed in extraarticular cells, human skin-derived fibroblasts were obtained from control donors and patients affected with the sporadic and familial varieties of CPPD (CPPD-S and CPPD-F) deposition. Intracellular PPi was elevated in both CPPD-S (P less than 0.05) and CPPD-F (P less than 0.01) fibroblasts compared with control fibroblasts. Ecto-NTPPPH activity was elevated in CPPD-S (P less than 0.01) but not CPPD-F. Intracellular PPi correlated with ecto-NTPPPH (P less than 0.01). Elevated PPi levels in skin fibroblasts may serve as a biochemical marker for patients with familial or sporadic CPPD crystal deposition disease; ecto-NTPPPH activity further separates the sporadic and familial disease types. Expression of these biochemical abnormalities in nonarticular cells implies a generalized metabolic abnormality.

Calcium Pyrophosphate↗
PubMed1984

A model for human calcium pyrophosphate crystal deposition disease: crystallization kinetics in a gelatin matrix.

A model for the deposition of calcium pyrophosphate dihydrate (CPPD) crystals in cartilage observed in human CPPD crystal deposition disease has been developed using diffusion of calcium and pyrophosphate ions through a denatured collagen matrix environment at physiologic pH. This model system uses biological grade gelatin and has allowed for the study of crystal deposition over a wide range of calcium and pyrophosphate concentrations, including physiologic levels. The model has reproducibly formed the two crystallographic dimorphs observed clinically: triclinic and monoclinic calcium pyrophosphate dihydrate. In addition, amorphous calcium pyrophosphate has been identified, and is the first species to form in the crystallization process and transforms to orthorhombic calcium pyrophosphate tetrahydrate. This in turn dissolves with a very localized increase in available pyrophosphate leading to the formation of triclinic and monoclinic calcium pyrophosphate dihydrate. The denatured collagen matrix has allowed for the formation of the two in vivo crystals at pyrophosphate concentrations lower than previously reported in solution studies.

Arthritis↗
PubMed1990

Calcium pyrophosphate crystal deposition: a kinetic study using a type I collagen gel model.

Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease is characterized by deposits of triclinic (t) and monoclinic (m) CPPD crystals in articular and fibrocartilage. Many investigators have attempted to model CPPD crystal growth using both solution and a variety of gel systems. We have investigated the effect of type I collagen fibrils on CPPD crystal nucleation and growth using an ionic diffusion model. Collagen was isolated from porcine menisci using a pepsin solubilization procedure and gelled in three layers, with one containing 10 mM pyrophosphate (PPi) plus physiologic ions, the middle containing only the ions, while the third contained 25 mM Ca plus physiologic ions. Initially, amorphorous calcium pyrophosphate formed at the Ca-PPi interface. Monoclinic CPPD crystallized in 6 weeks when the [Ca] was between 2 and 3 mM and the [PPi] was between 50 and 75 microM. At 13 weeks, t-CPPD formed when the [Ca] was also between 2 and 3 mM, but the PPi was less than 25 microM. One of the most striking differences between this system and all previous solution and gel model systems is the total absence of orthorhombic calcium pyrophosphate tetrahydrate (o-CPPT) from the gels made of collagen fibrils in near native conformation. Further, crystals of t-CPPD appear as large single crystals with the classic prismatic growth habit observed in vivo, and crystals of m-CPPD also evidence the in vivo rod habit. In contrast, the crystal growth habits of t-CPPD, m-CPPD, and o-CPPT grown in all of the other model systems never matched that observed in vivo. When compared to the previous studies, these results, particularly the crystal growth habit data, suggest that the native collagen fibrils themselves can nucleate CPPD crystal formation.

Animals↗
PubMed1991

Deposition of calcium pyrophosphate dihydrate crystals in the ligamentum flavum: evaluation with MR imaging and CT.

Four patients had spinal canal stenosis associated with deposition of calcium pyrophosphate dihydrate within the ligamentum flavum. Radiologic evaluation was performed with magnetic resonance imaging or computed tomography, and surgery was performed on all four patients. Pathologic examination of the surgical specimens demonstrated deposits of calcium pyrophosphate crystals within the ligamentum flavum. Focal enlargement of the ligamentum flavum was present in the cervical spine (n = 1), while a more diffuse, bilateral enlargement was identified in the lumbar spine (n = 3). Enlargement of the ligament either caused or was a component of spinal stenosis that caused neurologic signs or symptoms. Three of the patients had evidence of calcium pyrophosphate deposition elsewhere. Deposition of calcium pyrophosphate dihydrate within the ligamentum flavum causing either focal or diffuse enlargement can be associated with significant spinal stenosis.

Aged↗
PubMed1991

Calcium pyrophosphate dihydrate gout and other crystal deposition diseases.

The number of crystal or birefringent particles associated with arthritis is increasing, and a uniform taxonomy is needed. The term gout has been proposed as a generic term for these diseases based on historical, clinical, and crystallographic reasons. Calcium pyrophosphate dihydrate gout follows monosodium urate gout in frequency, and its spectrum of clinical manifestations continues to grow. Familial calcium pyrophosphate dihydrate gout was described for the first time in kindreds studied in England and Tunisia; new Jewish and Spanish kindreds were also reported. Type I collagen was shown to nucleate nativelike calcium pyrophosphate dihydrate crystals, and pyrophosphate elaboration was explored in cartilage explants in an attempt to reproduce the in vivo metabolic or endocrine disorders associated with calcium pyrophosphate dihydrate gout. The effect of pyrophosphatase and different cofactors such as magnesium in dissolving calcium pyrophosphate dihydrate crystals was investigated. High-resolution electron microscopy was used to study the interrelation between apatite and other basic calcium phosphate crystals in apatite gout. Raman microscopy was applied for the first time to identify crystals in biologic specimens. A simple and specific technique for basic calcium phosphate crystal identification is necessary to understand the relationship between different calcium phosphate crystals and osteoarthritis. Several reports about children and young patients with primary oxalate gout described the effect of oxalate on eyes, periodontal tissues, and bone. Multicenter studies showed poor results of renal transplantation, but favored combined liver and renal transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcinosis↗
PubMed1991

Calcium pyrophosphate dihydrate deposition disease: morphological and microanalytical features.

The light microscopic and polarization appearances of calcium pyrophosphate dihydrate crystal deposits in tissues are reviewed. In routine sections haematoxylinophilic crystalline deposits with a feathery or brush-like pattern are typical of calcium pyrophosphate dihydrate. Short rhomboidal crystals showing positive birefringence are seen on polarization; X-ray microanalytical and infrared spectroscopic data support the specificity of these appearances. The appearances of the crystal deposits in decalcified specimens are also described. We include six cases of calcium pyrophosphate dihydrate deposition within periarticular bone; to the best of our knowledge this has not previously been described.

Aged↗
PubMed1987

Effect of glycosaminoglycans on calcium pyrophosphate crystal formation in collagen gels.

Formation of calcium pyrophosphate dihydrate (CPPD) crystals in native collagen gels represent an in vitro model system for the study of pathological cartilage calcification. The conditions under which CPPD forms in collagen gels have been determined. At low Ca X pyrophosphate product, CPPD forms directly. At high Ca X pyrophosphate product, CPPD forms via the amorphous intermediate calcium magnesium pyrophosphate (CMPP). Chondroitin sulfate (CS) inhibits formation of CPPD by both pathways, but apparently by different mechanisms. Direct CPPD formation is inhibited with low potency by CS, apparently by binding of Ca2+ ions. Indirect formation of CPPD is inhibited with high potency by CS, apparently by stabilization of the CMPP intermediate. Comparison of the inhibition of direct CPPD formation by the two glycosaminoglycan species occurring in cartilage proteoglycan showed that CS is a more potent inhibitor than keratan sulfate (KS), in agreement with the greater Ca2+-binding affinity of CS. The increase in KS/CS ration which occurs in human hyaline cartilage with aging may facilitate deposition of CPPD crystals by decreasing the exclusion of pyrophosphate anions.

Calcium Pyrophosphate↗
PubMed1978

Calcium pyrophosphate dihydrate crystal formation in model hydrogels.

Using powder x-ray diffraction analysis, we studied calcium pyrophosphate crystal formation in silica and gelatin gels was well as in comparable aqueous solutions. We demonstrated that the physiological salts, monoclinic and triclinic calcium pyrophosphate dihydrate can be formed in gels and that gels do affect the type of crystals formed from ions in solution. These observations support our hypothesis that calcium pyrophosphate dihydrate crystal deposition in joints is regulated by the physical chemical gel state of the connective tissue matrix.

Calcium Pyrophosphate↗
PubMed1995

Tumoral calcium pyrophosphate dihydrate deposition disease mimicking a cervical spine neoplasm: case report.

A case of tumoral calcium pyrophosphate dihydrate crystal deposition disease involving the upper cervical spine is reported. It presented clinically, radiographically, and by preliminary intraoperative pathological evaluation as a possible malignant soft tissue tumor. An aggressive resection of the lesion was performed. This case differs from previous reports of calcium pyrophosphate dihydrate crystal deposition disease of the cervical spine by the size, location, and radiographic appearance of the lesion. We suggest that radical surgical procedures should not be performed without consideration of this diagnosis in lesions with similar presentations. A brief review of spinal and tumoral calcium pyrophosphate dihydrate crystal deposition is presented.

Adult↗
PubMed1995

Tophaceous pseudogout (tumoral calcium pyrophosphate dihydrate crystal deposition disease).

Most cases of calcium deposition seen radiologically in soft tissues are caused by calcium hydroxyapatite and occur either as a complication of trauma with associated necrosis (eg, fat necrosis), generalized connective tissue diseases (eg, scleroderma), metabolic disturbances (eg, hyperparathyroidism, familial hyperphosphatemia), sarcoidosis, myeloma, or metastases. Hydroxyapatite deposits are seen at many soft tissue sites, including joint capsules, ligaments, blood vessels, dermis, etc. On the other hand, deposits of calcium pyrophosphate are seen typically in the meniscus, articular cartilage, ligamentum flavum, and intervertebral disc. They usually are punctate or linear in distribution within the meniscus or parallel to the subchondral bone end plate. We report seven cases of massive focal calcium pyrophosphate dihydrate (CPPD) crystal deposition disease (tophaceous pseudogout) that occurred in atypical locations for CPPD. The ages of the patients ranged from 31 to 86 years (average, 60.7 years). One patient was male and six were female. The temporomandibular joint was involved in three patients and the metatarsophalangeal joint of the great toe was involved in two patients. The hip joint and cervical spine were involved in one patient each. A mass or swelling with or without pain was a common symptom. None of the patients in our series had clinical or radiographic evidence of CPPD crystal deposition disease in any other joints. Roentgenograms showed calcified lesions with a granular or fluffy pattern. Histologically, the lesions showed small or large deposits of intensely basophilic calcified material containing needle shaped and rhomboid crystals with weakly positive birefringence characteristic of CPPD. Foreign body granulomatous reaction to the CPPD deposition was constantly found. Chondroid metaplasia around and in the areas of CPPD deposition was observed commonly. Some of the chondroid areas showed cellular atypia in chondrocytes suggestive of a malignant cartilage tumor. It is important to recognize this rare form of CPPD crystal deposition disease and to identify the CPPD crystals in the calcified deposits, thus avoiding the misdiagnosis of benign or malignant cartilaginous lesions.

Adult↗
PubMed1981

Release of collagenase, neutral protease, and prostaglandins from cultured mammalian synovial cells by hydroxyapatite and calcium pyrophosphate dihydrate crystals.

Hydroxyapatite (HA) and calcium pyrophosphate dihydrate (CPPD) crystals were phagocytosed when added to cultured human rheumatoid or normal canine synovial cells. Collagenase and neutral protease secretion into the culture medium was increased 5- to 8-fold over control values in the presence of HA and increased 3-fold in the presence of CPPD crystals. HA but not CPPD crystals induced a 300-fold increase in human rheumatoid synovial cell culture fluid prostaglandin (PG) E2 levels and an 8-fold increase in PGF alpha levels. This mechanism may be important in the pathogenesis of the destructive arthropathies associated with HA and CPPD crystals.

Animals↗
PubMed2004

[Calcium pyrophosphate dihydrate-crystal induced arthropathy].

Calcium pyrophosphate dihydrate (CPPD) crystal induced arthropathy (CPPD-CA; systemic articular chondrocalcinosis) characterized by deposition of CPPD-crystals in fibro- and hyaline cartilage, joint capsule and periarticular tissues is associated with a variable clinical spectrum of inflammatory degenerative and occasionally destructive joint and vertebral manifestations including neurologic complications and rarely tophaceous-tumoral tissue calcifications. Microcrystal formation in the extracellular matrix of cartilage and tendons is based on genetic and acquired dysregulation of chondrocyte pyrophosphate metabolism and presumably linked to gene mutants on the short arm of chromosome-5 (gene locus 5p15.1 and ANKH gene). Idiopathic disease occurs rarely in hereditary-familial and frequently in sporadic manifestation with increasing prevalence due to aging; a secondary form is significantly related to endocrine and metabolic disorders (as to hyperparathyroidism, hemochromatosis etc.). The impact of the clinical syndrome in practice is important in differential diagnosis of age related conditions like acute mono- or oligoarthritis, systemic osteoarthritis and polymyalgia rheumatica. Actual treatment ignores established prevention of systemic cartilage calcification and is oriented to symptomatic relief.

Arthrography↗
PubMed1996

The interaction of monoclinic calcium pyrophosphate dihydrate crystals with neutrophils.

Monoclinic calcium pyrophosphate dihydrate (m-CPPD) crystals were synthesized and characterized using physical methods, IgG binding to m-CPPD crystals was quantitated, and the effect of IgG or plasma opsonization on m-CPPD-induced neutrophil activation was determined. Adsorption of IgG to crystals was measured using fluorescent-labelled FITC-IgG. Neutrophil activation by uncoated m-CPPD and crystals precoated with IgG or plasma was measured using luminol-enhanced chemiluminescence, superoxide anion generation, and myeloperoxidase release. m-CPPD bound small (compared to triclinic CPPD) but significant amounts of IgG and induced a strong activation of neutrophils at low concentrations of crystals. The rate and extent of chemiluminescence, superoxide anion production, and degranulation was not affected by precoating m-CPPD crystals with IgG during the early phase of neutrophil responses, but was inhibited by the precoating of crystals with plasma.

Adsorption↗
PubMed1995

[The solubility of calcium pyrophosphate dihydrate crystals].

The solubility of calcium pyrophosphate dihydrate crystals (CPPD crystals), which cause pseudogout, was studied in vitro and vivo. The in vitro experiment using 0.1 M tris buffer and 0.2 M glycine buffer indicated that changes in pH and pyrophosphatase activity played a major role in the solubility of CPPD crystals. An experiment using the synovial fluid from patients with pseudogout, rheumatoid arthritis, and from those with osteoarthritis suggested that changes in the synovial fluid pH due to inflammation affected the solubility of these crystals. In addition, an experiment using the air pouch in rat showed that inflammation due to the CPPD crystals was maximum at about 9 hours after CPPD injection, and that inflammatory cells appearing at this time then had a major influence on the crystals' solubility. From these results, it appeared that CPPD crystals released into the joint cavity were mostly dissolved by inflammatory cells, but that crystal dissolution was also affected by changes in the synovial fluid itself, particularly by a change in pH.

Animals↗