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PubMed1984

Pyrophosphate arthropathy as a late complication of juvenile chronic arthritis.

Pyrophosphate arthropathy is an age-related disease rarely seen in those under 45 years of age. We report 2 patients with early onset pyrophosphate arthropathy in joints previously affected by juvenile chronic arthritis. This previously undescribed association supports the hypothesis that joint damage may predispose to calcium pyrophosphate dihydrate crystal deposition and lead to secondary pyrophosphate arthropathy.

Adult↗

PubMed1991

Synovial fluid ATP: a potential substrate for the production of inorganic pyrophosphate.

The enzyme nucleoside triphosphate pyrophosphohydrolase (NTPPPH) is present in all joint fluids and on intraarticular cells. It generates inorganic pyrophosphate (PPi) from nucleoside triphosphate substrate, thus serving as a potential source of the PPi which forms in the cartilages of patients with calcium pyrophosphate dihydrate (CPPD) crystal deposition. NTPPPH is also important in matrix vesicle induced calcification with basic calcium phosphate (BCP) crystals. An articular substrate for this enzyme was sought. ATP was measured in the joint fluids from 107 patients with various forms of arthritis. Synovial fluid ATP levels were higher in patients with CPPD deposits than in osteoarthritis (p less than 0.02) or rheumatoid arthritis (p less than 0.002). ATP also correlated with PPi concentration (p less than 0.05) and with the presence of BCP crystals (p less than 0.05), but not with cellularity of the fluid, NTPPPH activity, or age of the donor. This substrate for NTPPPH may contribute to CPPD crystal deposition by generating PPi and may stimulate matrix vesicle induced formation of BCP crystals in several forms of arthritis.

Adenosine Triphosphate↗

PubMed1985

Amyloid in intervertebral discs. A histopathological investigation of intervertebral discs from 30 randomly selected autopsies.

Material from intervertebral discs obtained from 30 randomly selected autopsies was examined histologically for amyloid deposits. Various degrees of amyloid degeneration were found in the disc tissue from 28 of the autopsies. In the annulus fibrosus, the amyloid was lying between the thick bundles of collagen fibers, compared to a more diffuse nodular distribution in the nucleus pulposus, frequently in close relation to chondrocytes. With regard to the lumbar discs, a significant correlation was found between the occurrence of islands of chondroid tissue in the annulus fibrosus and amyloid degeneration. Significantly more amyloid was observed in disc tissue in older age groups, while the amount of amyloid was similar in discs from men and women. Calcium-pyrophosphate-dihydrate (pyrophosphate) was found in the tissue of 6 of the 7 women over the age of 70. Calcium phosphate was seen in 22 of the autopsies--more frequently in the annulus fibrosus than in the nucleus pulposus. There was no topographical relationship between calcium phosphate and amyloid.

Adult↗

PubMed1979

[Study of cellular elements in synovial fluid in scanning electron microscopy].

Scanning electron microscopy allows a tridimensional morphological study of the cellular elements of the pathological human synovial fluid. The cells are grouped into two populations: macrophage cells and round cells, whose differentiation is more difficult: polynuclears, lymphocytes and synovial cells. The combination of scanning electron microscopy and X-ray diffraction makes it possible to describe and indentify crystals of sodium urate and of triclinical, dehydrated calcium pyrophosphate.

Arthritis, Rheumatoid↗

PubMed2006

Osteopontin promotes pathologic mineralization in articular cartilage.

Calcium pyrophosphate dihydrate (CPPD) crystals are commonly found in osteoarthritic joint tissues, where they predict severe disease. Unlike other types of calcium phosphate crystals, CPPD crystals form almost exclusively in the pericellular matrix of damaged articular cartilage, suggesting a key role for the extracellular matrix milieu in their development. Osteopontin is a matricellular protein found in increased quantities in the pericellular matrix of osteoarthritic cartilage. Osteopontin modulates the formation of calcium-containing crystals in many settings. We show here that osteopontin stimulates ATP-induced CPPD crystal formation by chondrocytes in vitro. This effect is augmented by osteopontin's incorporation into extracellular matrix by transglutaminase enzymes, is only modestly affected by its phosphorylation state, and is inhibited by integrin blockers. Surprisingly, osteopontin stimulates transglutaminase activity in cultured chondrocytes in a dose-responsive manner. As elevated levels of transglutaminase activity promote extracellular matrix changes that permit CPPD crystal formation, this is one possible mechanism of action. We demonstrate the presence of osteopontin in the pericellular matrix of chondrocytes adjacent to CPPD deposits and near active transglutaminases. Thus, osteopontin may play an important role in facilitating CPPD crystal formation in articular cartilage.

Adenosine Triphosphate↗

PubMed1993

Calcium crystal deposition in the ligamentum flavum of the cervical spine.

This article reports eight patients who underwent posterior decompressive surgery for myeloradiculopathy caused by calcium crystal deposition in the ligamentum flavum of the cervical spine. All were women with an average age of 72 years and showed neurologic improvement postoperatively. Four patients had diabetes mellitus, and knee meniscus calcification on radiographs were noted in four patients. The ligamentum flavum of C5-6 and C6-7 were sites frequently involved. Crystallographic examination confirmed resected deposits as calcium pyrophosphate dihydrate crystal in all patients and additional hydroxyapatite crystal in two. Histology confirmed marked degeneration in elastic fibers about the calcium deposits. This pathologic condition is possibly spinal manifestation of systemic calcium crystal deposition disease.

Aged↗

PubMed1987

Radiologic features of a pyrophosphate-like arthropathy associated with long-term dialysis.

In a series of 28 long-term dialysis patients with musculoskeletal complaints, the radiologic findings in six cases resembled those occurring in the arthropathy of idiopathic calcium pyrophosphate dihydrate deposition (CPPD) disease. These findings included osteophytes, subchondral cysts, and cartilage loss in the metacarpophalangeal joints, patellofemoral joints, wrists, and shoulders. Chondrocalcinosis was present in three of the six cases. There were no significant differences in renal function or levels of serum calcium, phosphorus, iron, ferritin, aluminum, or parathormone between these patients and a control group matched for sex and age. Long-term dialysis may be associated with a metabolic arthritis similar to the arthritis which occurs in CPPD deposition disease. The etiology may include deposition of CPPD crystals, hydroxyapatite, or other calcium-containing substances in joints, or it may be related to a number of dialysis-induced metabolic abnormalities.

Arthritis↗

PubMed1991

Identification of pathological mineral deposits by Raman microscopy.

Raman microscopy--the analysis of scattered photons after excitation--is well established in non-biological sciences for the identification of crystals. It shows promise in biological (clinical) specimens also, as demonstrated here in studies of synovial fluid, synovium, and gouty tophus, selected for their known content of sodium urate and calcium pyrophosphate crystals.

Aged↗

PubMed1985

Apatite-type crystal deposition in arthritic cartilage.

Osteoarthritis or 'Joint Failure' is a multi-factorial disease with a final common pathway of cartilage degeneration and bone eburnation. The association of arthritic disease and joint degeneration with the deposition of sodium urate crystals in gout and calcium pyrophosphate crystals in pseudogout (chondrocalcinosis) is clinically well established. Electron microscopy coupled with electron probe analysis has revealed the presence of various other calcium phosphate crystals in joint tissues and fluids. We have found three new morphological types of apatite crystals in human articular cartilage which are too small to be detected by X-rays of human joints or even by light microscopy of joint tissues. Two morphologically distinct types of apatite crystals in articular cartilage are associated with extracellular matrix vesicles formed from the cell processes of chondrocytes. 'Cuboid' crystals, which are found in the pericellular regions near the surface zone of articular cartilage, appear to be a variant of apatite and may even be 'Whitlockite' because there are traces of magnesium present. There are increased numbers of these microscopic 'cuboid' crystals (Type II) and Mineral Nodules (Type I) in arthritic cartilage and this is coupled with increased numbers of matrix vesicles and alkaline phosphatase activity. Clusters of fine needle-shaped apatite crystals (Type III) found on the surface of articular cartilage are not associated with matrix vesicles. Thus some forms of osteoarthritis are closely associated with apatite type crystal deposition and may imply abnormal mineral formation in articular cartilage as a pathogenic mechanism.

Apatites↗

PubMed2005

[Chondrocalcinosis (pseudogout) after surgical treatment of primary hyperparathyroidism. Report of a case and review of the literature].

We are reporting the case of a 61-year-old female who developed an acute arthritis following parathyroidectomy because a primary hyperparathyroidism. The diagnosis of chondrocalcinosis or pseudogout was made by the clinical presentation, radiologic findings and demonstration of synovial fluid crystals of calcium pyrophosphate dihydrate. Rapid drops in serum calcium levels after removal of the adenoma may precipitate these acute articular inflammatory attacks that are not so uncommon as we can recognize if a bibliographic review about that association is performed.

Chondrocalcinosis↗

PubMed1990

Stimulation of pyrophosphate production in articular cartilage by a platelet-derived factor is independent of mitogenesis.

The disordered production of extracellular inorganic pyrophosphate (PPi) by cartilage contributes to calcium pyrophosphate dihydrate crystal formation and associated diseases. We have previously shown that a factor(s) derived from human platelets markedly stimulates the accumulation of PPi in the media of porcine articular cartilage in organ culture. This is the first known physiologic modifier of PPi production by cartilage. We report herein that platelet derived growth factor (PDGF) is not the platelet factor responsible for PPi stimulation and that the active factor is not mitogenic for chondrocytes. PDGF added to the media of articular cartilage explants in the presence of 0.5% (platelet-poor) plasma (PPP) produces 3.92 +/- 1.6 mumol/L PPi compared with 2.85 +/- 0.7 mumol/L PPi in cartilage exposed to PPP alone. The platelet extract (PE) and PDGF are mitogenic for adult articular chondrocytes in high-density monolayer cultures. Anti-PDGF antibodies block the mitogenic effects of PDGF and PE. The uptake of thymidine labeled with tritium is 157% of control in cells exposed to PE, PPP, and polyclonal goat immunoglobulin G (IgG); 114% of control in cells exposed to PE, PPP, and anti-PDGF antibody; 148% of control in cells treated with PDGF, PPP, and goat IgG; and 98% of control in cells treated with PDGF, PPP, and anti-PDGF antibody. However, anti-PDGF antibody has no effect on PPi accumulation. PPi levels are 17.22 +/- 1.6 mumol/L in media from cartilage treated with PPP, goat IgG, and PE and 17.62 +/- 2.2 mumol/L in cartilage exposed to PE, PPP, and anti-PDGF antibody. We have further characterized the platelet factor responsible for the stimulation of PPi by cartilage. It is not mitogenic for chondrocytes, and it is not PDGF.

Animals↗

PubMed1994

Probenecid inhibits transforming growth factor-beta 1 induced pyrophosphate elaboration by chondrocytes.

OBJECTIVE: The elaboration of excess extracellular inorganic pyrophosphate (ePPi) by cartilage contributes to calcium pyrophosphate dihydrate (CPPD) crystal deposition disease. Transforming growth factor-beta 1 (TGF beta 1) is the only defined physiologic stimulant of cartilage ePPi elaboration. The mechanism of ePPi generation by chondrocytes is unknown, but current evidence suggests that TGF beta 1 induced ePPi is made intracellularly. An active transport mechanism such as an anion transporter would then be necessary to export ePPi to the matrix where crystals form. We determined the effect of probenecid (PB), an anion transport inhibitor, on TGF beta 1 induced ePPi elaboration. METHODS: Porcine hyaline articular chondrocytes in high density monolayer cultures were exposed to serum-free media with and without TGF beta 1 and/or PB. ePPi was measured in the media after 48-96 h of exposure. Cell injury was measured by examining the release of 3H-deoxyglucose from chondrocytes. The activity of the ePPi generating ectoenzyme nucleoside triphosphate pyrophosphohydrolase (NTPPPH) and media lactate concentrations were measured with standard colorimetric assays. As PB may inhibit phosphodiesterase (PDE), its effects on ePPi generation were compared with isobutylmethylxanthine (IBMX), a specific PDE inhibitor. RESULTS: PB inhibited TGF beta 1 induced ePPi elaboration by chondrocytes. PB did not cause membrane injury or decrease NTPPPH activity. Lactate production was decreased by PB but did not correlate with the effects of PB on ePPi elaboration. IBMX did not inhibit TGF beta 1 effect on ePPi elaboration. CONCLUSION: PB blocks TGF beta 1 induced ePPi elaboration. This effect is independent of cell membrane injury, decreased NTPPPH activity, or PDE inhibition. Our data implicate a role for anion transport in TGF beta 1 induced ePPi elaboration, and suggest a potential therapy for CPPD disease.

1-Methyl-3-isobutylxanthine↗

PubMed1993

Association of radiographic changes of osteoarthritis, symptoms, and synovial fluid particles in 300 knees.

Associations between compartmental distribution of radiographic changes of osteoarthritis (OA), individual features of OA (joint space loss, sclerosis, cyst, osteophyte; each scored 0-3), and presence of synovial fluid calcium particles (calcium pyrophosphate dihydrate (CPPD) crystals identified by polarised light microscopy and other calcium particles by alizarin red positivity (ARP) were sought in 300 osteoarthritic knees (178 patients; mean age 72, range 33-96 years). Patients whose knees were symptom free as well as those with symptoms were included. Osteoarthritis of two or three compartments but not unicompartmental OA was associated with the presence of CPPD or ARP. Involvement of any compartment (not just patellofemoral), and higher mean scores for both total and individual osteoarthritis changes (except cysts) was associated with CPPD and ARP; CPPD, but not ARP, was associated with symptoms: knees reported as having symptoms had higher mean total OA scores. Femoral cortical erosion, found more often in women, was associated with higher mean total OA score at the patellofemoral compartment but not with the presence of particles. Attrition, remodelling, and chondrocalcinosis (each scored as present or absent) occurred more often in knees with CPPD. Age did not correlate with any aspect of the OA score. This study confirms the association of calcium particles with the process of OA. Unlike previous studies confined to symptomatic knees, a radiographic pattern specific to CPPD ('pyrophosphate arthropathy') did not emerge.

Adult↗

PubMed1985

Amyloid deposits in human knee and hip joints.

A systematic search for articular amyloidosis was carried out on both knees of 53 autopsy cases and on 26 femoral heads resected during surgery for hip prosthesis. Typical amyloid deposits exhibiting green apple birefringence following Congo red staining and thioflavin T fluorescence were found in 58.5% and 29% of the cases, in the knee and hip joint respectively. They occurred more frequently in articular cartilage than in the synovium, and in elderly subjects more than young ones. In the knee joint, the osteoarthritic changes and to a minor extent synovial inflammation appear to be positively correlated for the presence of intraarticular amyloid deposits. Such a correlation was not observed for the presence of calcium pyrophosphate dihydrate crystal deposits.

Aged↗

PubMed1995

[Calcinosis of the meniscus. Morphologic and roentgenographic findings for zonal classification].

Primary and secondary meniscal chondrocalcinoses lead to typical changes in X-ray pictures of isolated menisci. Combined X-ray, light and electron microscopic examination of the four menisci in 70 autopsy cases showed calcifications in 13 cases (18.6%). Three types of calcification could be discriminated with the help of topographical and morphological criteria: Type 1 A: disseminated calcification. All four menisci were affected equally. Crystals of calcium pyrophosphate dihydrate (CPPD) were found on light and electron microscopy. Energy-dispersive X-ray analysis (EDX) showed the crystal deposits to consist of 46.5% calcium and 53.5% phosphorus. Type 1 B: Calcification occurring in limited areas. A calcification was found which did affected neither a whole meniscus nor all four menisci of any "quartet" observed. Crystals were found next to areas of stronger meniscal degeneration. EDX showed the same results described for type 1 A. Type 2: Confluent calcification. A cloud-like diffuse calcification was discerned on the X-ray pictures. Light and electron microscopically pseudocystic structures appeared which contained a fine granular amorphous material. No crystals were found. The structures appeared in the neighbourhood of necrotic fibres. EDX showed 44% calcium, 51.2% phosphorus, 2.8% sulphur, 0.74% magnesium and 0.6% potassium. The findings lead to the conclusion that calcification type 1 A represents primary chondrocalcinosis, whereas type 1 B corresponds to secondary chondrocalcinosis. Type 2 was identified as postnecrotic, dystrophic calcification. Careful analysis of X-ray pictures of isolated menisci can yield useful information concerning pathogenetic factors of meniscal calcification.

Calcium Pyrophosphate↗

PubMed1977

[Physiopathology of articular chondrocalcinosis].

The physiopathological mechanisms leading to precipitation of pyrophosphate in the articular cartilage remain unclear. Numerous findings suggest an error in pyrophosphate metabolism: excessive production or defective degradation, a primary modification of the fundamental substance leading to crystallization, a chondrocyte dysfunction being a possible cause of these two anomalies. The relationships between deposition of calcium pyrophosphate and changes in the subchondral osseous plaque common to several metabolic diseases are even more mysterious.

Calcium Pyrophosphate↗

PubMed1988

Pathology of crystal deposition diseases.

Pathologic examinations of joint fluid and articular tissues can be valuable in diagnosis and evaluation of pathogenesis of crystal-associated arthropathies provided that careful attention is paid to processing of tissues. Urates, calcium pyrophosphate, and apatite-like crystals are most common in human lesions and are most widely studied.

Apatites↗

PubMed1995

Gout or 'pseudogout': how to differentiate crystal-induced arthropathies.

Gout is an inflammatory joint disease that primarily affects middle-aged men and postmenopausal women. It is characterized by severe pain and erythema in the big toe and other affected joints. Acute gout may be triggered by diuretics, aspirin, minor trauma, or acute illness. The presence of monosodium urate crystals within phagocytes from synovial fluid aspirates is almost always diagnostic. Calcium pyrophosphate deposition disease ("pseudogout") usually affects larger joints and often follows trauma, surgery, or ischemic heart disease. Microscopic examination of crystals under compensated polarized light is used to differentiate gout and pseudogout. Disorders involving basic calcium phosphate are often more difficult to diagnose and treat but are also less likely to be disabling.

Adult↗