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Formation of calcium pyrophosphate crystals in vitro: implications for calcium pyrophosphate crystal deposition disease (pseudogout).

Little is known about how calcium pyrophosphate dihydrate (CaPPD) crystals form in vivo and give rise to chondrocalcinosis or pseudogout (pyrophosphate arthropathy or calcium pyrophosphate crystal deposition disease). In this study a simple method has been devised to define the conditions necessary for the deposition of crystals in vitro. Crystal formation is monitored by (45)Ca in the presence of 1.5 mmol/l Ca and increasing concentrations of inorganic pyrophosphate (PPi) under simulated physiological conditions of pH and ionic strength. Concentrations of PPi required to initiate crystal formation were about 40 mmol/l in the absence and 175 mmol/l in the presence of 0.5 mmol/l Mg(2+) at pH 7.4. Less PPi was required at higher pH values. The naturally occurring monoclinic and triclinic forms of CaPPD were produced after prolonged incubation in vitro, but the initial deposits were amorphous or orthorhombic. The physiological significance of these observations is discussed. Since much higher concentrations of PPi are required to form crystals in vitro than are found to occur naturally in synovial fluids from patients with pyrophosphate arthropathy, it is suggested that crystals are more likely to deposit initially within cartilage and that nucleating mechanisms may be important in vivo. Since other workers have observed a slow interconversion of other calcium pyrophosphate crystal forms into monoclinic and triclinic allomorphs under laboratory conditions, the reason why only these 2 forms occur under clinical conditions may reflect the long time available in vivo for the formation of crystals.

Calcium Pyrophosphate

Pyrophosphate, phosphate ion interaction: effects on calcium pyrophosphate and calcium hydroxyapatite crystal formation in aqueous solutions.

The relationship between ambient ionic conditions that favor pyrophosphate (PPi) versus phosphate (Pi) biomineralization is important to understanding the pathogenesis of chondrocalcinosis. We studied aqueous solutions at pH 7.4, 37 degrees C, [Na+] = 140 mM, [Mg+ +] = 0.5 mM, [Ca+ +] = 1.0 or 1.5 mM over a range of pyrophosphate and phosphate concentrations to determine the effect of different ambient concentrations and ratios of Pi/PPi on calcium pyrophosphate dihydrate (CPPD) and calcium hydroxyapatite (HA) crystal formation. We found that the Pi/PPi ratio is an extremely important determinant of the crystal product formed. At low [Pi], CPPD crystal formation is partially inhibited by Pi; at higher [Pi], calcium pyrophosphate, calcium phosphate and calcium pyrophosphate-phosphate complexes amorphous to x-ray diffraction are formed; whereas at still higher [Pi], HA crystal formation partially inhibited by PPi. We conclude that CPPD forms when the ratio [Pi]/[PPi] less than 3 and HA forms when [Pi]/[PPi] greater than 100.

Calcium Pyrophosphate

Calcium pyrophosphate and pseudogout.

Calcium pyrophosphate deposition disease (CPDD) is a condition in which calcium pyrophosphate dihydrate crystals are deposited in joint articular cartilage, menisci, and synovium. The main clinical presentations of CPDD are chondrocalcinosis--calcification of cartilage, pseudogout--acute joint inflammation due to crystal-induced synovitis, and pyrophosphate arthropathy--degenerative joint disease similar to osteoarthritis associated with calcium pyrophosphate crystal deposition. The clinical importance of CPDD for the arthroscopist is the ability to recognize the condition so that appropriate treatment can be instituted. Arthroscopy is valuable for diagnosis as well as lavage and intraarticular debridement or meniscectomy. Tissue removed for microscopic examination should be sent to the laboratory in saline, since formalin dissolves the crystals. Postarthroscopy treatment of CPDD should include oral antiinflammatory medication. Asymptomatic chondrocalcinosis does not require treatment.

Aged

Simultaneous occurrence of calcium pyrophosphate dihydrate and basic calcium phosphate (hydroxyapatite) crystals in a knee.

An 82-year-old man developed periarticular roentgenographic calcifications of the knee joint. Fragments of meniscus and peritendinous tissue were collected during total knee arthroplasty. Crystals were released from tissues by collagenase digestion. Calcium pyrophosphate dihydrate crystals were identified in the meniscus, and basic calcium phosphate crystals were identified in the peritendinous tissue. Methods of crystal identification included compensated polarized light microscopy, scanning electron microscopy with X-ray energy dispersive analysis, and X-ray diffraction.

Aged

Triple crystal disease: monosodium urate monohydrate, calcium pyrophosphate dihydrate, and basic calcium phosphate in a single joint.

A 49 year old man is described with a polyarticular arthritis. Synovial fluid aspirated from the knee joint showed monosodium urate monohydrate and calcium pyrophosphate dihydrate by polarised light microscopy. Additionally, diphosphonate binding and scanning electron microscopy with energy dispersive analysis showed that basic calcium phosphate crystals were also present. This appears to be the first report of three crystals occurring simultaneously in a single joint.

Arthritis

Wrist arthropathy in calcium pyrophosphate dihydrate deposition disease.

Calcium pyrophosphate dihydrate deposition disease is associated with chondrocalcinosis and a characteristic radiographic abnormality. In the wrist this abnormality consists of radiocarpal joint narrowing, sclerosis, and subchondral cystic degeneration of the carpal bones. These changes sometimes occur in the absence of chondrocalcinosis. Two investigate the significance of this occurrence, 18 patients with the radiographic abnormality of radiocarpal joint narrowing, sclerosis, and subchondral cystic degeneration were examined. Six had neither local wrist nor distant chondrocalcinosis. Five of the latter had wrist arthrocentesis and 4 had calcium pyrophosphate dihydrate crystals. Calcium pyrophosphate dihydrate deposition disease can occur in the absence of chondrocalcinosis and the diagnosis is strongly suggested by a characteristic radiographic picture.

Adult

Rhesus monkeys (Macaca mulatta) as a model for calcium pyrophosphate dihydrate crystal deposition disease.

Calcium pyrophosphate dihydrate crystal deposition disease (CPDD) was recognized in 4 of 30 free-ranging rhesus macaques. By means of tissue radiography, focal radiodensities were noted in lumbar intervertebral discs, menisci, and articular cartilage. Crystal deposits were identified as calcium pyrophosphate dihydrate (Ca2P2O7 X 2H2O) by means of X-ray diffraction. The pathogenesis of calcium pyrophosphate dihydrate arthropathy in man remains elusive. However, with the recognition of this arthritis in a well defined population of aged nonhuman primates, a model now exists to facilitate the study of this disease.

Animals

Inorganic pyrophosphate in metabolic diseases predisposing to calcium pyrophosphate dihydrate crystal deposition.

Inorganic pyrophosphate (PPi) levels were estimated by radiometric assay in urine and in synovial fluid (SF) from asymptomatic, nonarthritic knees of patients with untreated metabolic disease and normal controls. SF PPi was significantly elevated in patients with hyperparathyroidism (mean +/- SEM 19 +/- 3 microM; n = 9), hemochromatosis (23 +/- 5 microM; n = 6), and hypomagnesemia (27 +/- 0.1 microM; n = 2) compared with normal subjects (10 +/- 0.5 microM, n = 50), and was low in patients with hypothyroidism (4.2 +/- 2.3 microM; n = 11) (P less than 0.05 all comparisons). Urinary PPi was elevated only in those with hypophosphatasia. Local elevation of ionic PPi may be relevant to the mechanism of crystal formation in metabolic diseases predisposing to calcium pyrophosphate dihydrate (CPPD) crystal deposition. The finding of low SF PPi levels in patients with hypothyroidism further questions the association between this condition and CPPD.

Adult

Studies on the clearance of calcium pyrophosphate crystals from facsimile synovium.

Calcium pyrophosphate dihydrate crystals have been injected into the air pouch model of facsimile synovium. At various time intervals after crystal injection both infiltrating exudate cells and lining tissue were examined for the presence of crystalline material. The results show that the crystals are initially engulfed by mononuclear cells and to a lesser extent by polymorphonuclear cells in the exudate. Later, crystals became embedded in the lining tissue either within mononuclear cells or as crystal masses confined within granulomas. These studies suggest that the mesenchymal cells ( facsimile synovium) lining rat air pouches can clear calcium pyrophosphate dihydrate crystals from the air pouch cavity. It is therefore inferred that crystals found in the lining of human joint synovium may be incorporated therein by a similar mechanism.

Air

Calcium pyrophosphate dihydrate crystal deposition disease as a cause of lumbar canal stenosis.

STUDY DESIGN: This study measured the incidence of calcium pyrophosphate dihydrate crystal deposition in specimens of ligamenta flava in consecutive patients undergoing decompressive laminectomy between 1984 and 1991. The results were compared to determine the difference between calcium pyrophosphate dihydrate-negative patients with lumbar canal spinal stenosis. OBJECTIVES: The results were compared with cadaver specimens and literature values to determine if calcium pyrophosphate dihydrate crystal deposition disease contributes to the thickening of the ligamentum flavum and thereby contributes to spinal stenosis. SUMMARY OF BACKGROUND DATA: Calcium pyrophosphate dihydrate crystal deposition disease has been described in the axial skeleton. Hypertrophy of the ligamentum flavum has been suggested to contribute to stenosis. The association of calcium pyrophosphate dihydrate disease and hypertrophied ligamenta flava has not been fully defined nor linked to neurologic symptoms and signs. METHODS: The incidence of calcium pyrophosphate dihydrate crystal deposition in specimens of ligamenta flava obtained from four groups was measured: specimens obtained during surgery from 102 consecutive patients undergoing decompression laminectomy between 1984 and 1991, 47 additional pathologic specimens of ligamentum flavum tested between 1984 and 1991, 222 calcium pyrophosphate dihydrate-positive Pathology Department specimens collected between 1980 and 1991, and, as control specimens from 20 cadavers. The associated patient histories were reviewed for the first two groups; no histories were available for the cadaver group. RESULTS: The incidence of calcium pyrophosphate dihydrate crystal deposition was 24.5% in the ligamentum flavum among the surgical patients, 31% among the Pathology Department specimens, 33.8% among the calcium pyrophosphate dihydrate-positive Pathology Department specimens, and 5% among the cadavers. No associated medical conditions with calcium pyrophosphate dihydrate crystal deposition were found among the medical histories. Patients with the symptoms of spinal stenosis who were also calcium pyrophosphate dihydrate-negative patients with symptoms of less than 6 months' and less than 24 months' duration (P < 0.001). Except for time to presentation, calcium pyrophosphate dihydrate-negative patients had similar signs and symptoms of lumbar canal spinal stenosis. Having previous spine surgery did not produce a statistically significant risk of having calcium pyrophosphate dihydrate crystal deposition. No specific laboratory tests were found to be of predictive value. CONCLUSIONS: These findings suggest that calcium pyrophosphate dihydrate crystal deposition may indeed be associated with the thickening of the ligamentum flavum, if so, patients may benefit from medical treatment before undergoing surgical treatment of lumbar canal spinal stenosis.

Aged

Quantification of human plasma inorganic pyrophosphate. I. Normal values in osteoarthritis and calcium pyrophosphate dihydrate crystal deposition disease.

The methodologic variables of the UDPG pyrophosphorylase method for analysis of inorganic pyrophosphate (PPi) levels in biologic fluids are described. Use of a tourniquet in collection of blood specimens elevated plasma PPi levels from 35% to 55% above control values and may explain the differences in published normal values. The sodium pyrophosphate decahydrate used to prepare the standard solution lost 8 waters of hydration after dessication, which could result in the calculation of spuriously elevated PPi levels. Normal plasma PPi concentration was 2.18 muM with a range (95% confidence limits) of 0.58-3.78 muM. Comparison of plasma PPi in normal subjects, patients with primary osteoarthritis, and patients with calcium pyrophosphate dihydrate deposition disease revealed no significant intergroup differences.

Blood Specimen Collection

[Clinico-radiologic aspects of calcium pyrophosphate dihydrate deposition disease].

Calcium pyrophosphate dihydrate crystal deposition disease is a clinical condition characterised by Gout-like synovitis (pseudogout), calcification on and around the joints and an arthropathy that is radiologically similar to osteoarthritis (chronic pyrophosphate arthropathy). Though all these radiological clinical aspects may coexist in the same patient this is often not the case. An examination of the X-ray data on the 68 cases studied which were diagnosed on the basis of the criteria proposed by McCarty, shows that the disease is relatively common especially in the over-fifties. When chronic pyrophosphate arthropathy is the only clinical manifestation of the disease differential diagnosis from the osteoarthrosis so common in the elderly is difficult and depends on the greater severity and progression of the joint damage that may often affect joints not subjected to weight such as the shoulder, unlike what happens in osteoarthritis.

Aged

Calcium pyrophosphate dihydrate deposition in lumbar disc fibrocartilage.

Calcium pyrophosphate dihydrate deposits were found in the lumbar disc fibrocartilage in 4 patients undergoing surgery for spinal cord or nerve root compression. All of the patients had prior surgery at the same lumbar area. None of the patients had the articular or roentgenographic manifestations of calcium pyrophosphate deposition disease (pseudogout). Andres and Trainer have recently reported 7 similar patients. Calcium pyrophosphate dihydrate deposition in axial skeleton fibrocartilage may be a common finding in patients undergoing repeat spinal surgery.

Adult

The effect of calcium and magnesium ions on calcium pyrophosphate crystal formation in aqueous solutions.

Calcium pyrophosphate crystal formation has been associated clinically with hypercalcemic states (hyperparathyroidism) and hypomagnesemia. We studied aqueous solutions at pH 7.4, 37 degrees C, [Na+] = 140 nM over a range of calcium chloride/magnesium chloride/sodium pyrophosphate concentrations to determine the effect of calcium and magnesium ions on crystal formation. We found that CPPD(T) and CPPD(M) could form under different ionic conditions. Low [Mg++] and [PPi] favoured CPPD(T) whereas higher [Mg++] and [PPi] favoured CPPD(M). At [Mg++] = 1.0 mM a calcium magnesium pyrophosphate crystal phase designated CMPP2 formed. As [Mg++] affects the crystal phase formed more than equimolar [Ca++], we conclude that ionic magnesium deficiency may be a clinically important determinant in calcium pyrophosphate dihydrate crystal formation.

Calcium

[Arthropathies due to calcium pyrophosphates].

Articular chondrocalcinosis results from the deposits of calcium pyrophosphate microcrystals in the articular hyalin and fibrocartilages, the synovium and at times the tendons. In our area it is seen most frequently as isolated cases in the elderly and may be asymptomatic. When the affected joints present clinical manifestations, they vary from acute to subacute or chronic recurrent arthritis. A marked articular destruction can be observed in some cases. There is a classical radiological picture: linear opacities are most frequently seen localized in the mid-zone layer of the hyalin cartilage running parallel to but at a certain distance from the bone cortex. A part of our research has shown that in contrast to urate gout, articular chondrocalcinosis results from a metabolic disturbance of the calcium pyrophosphate localized almost exclusively in the same articular structures. Precise information is lacking at the present time to explain why calcium pyrophosphate mycrocrystals accumulate in the cartilage, the synovium and at times at the tendons; nor do we understand the precise role played by the pyrophosphate in bone and cartilage destruction.

Aged