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PubMed1991

Survival of calcium pyrophosphate crystals in stored synovial fluids.

Eleven synovial fluids containing calcium pyrophosphate dihydrate (CPPD) were examined repeatedly over an eight week period to assess whether storage conditions and duration influenced the number of crystals present. Aliquots of each fluid were stored at room temperature, 4 degrees C, and -70 degrees C. At -70 degrees C there was no change in crystal count after eight weeks' storage. At room temperature and 4 degrees C crystal counts declined slowly over the eight week period, though CPPD crystals were still readily apparent after eight weeks in 10/11 (4 degrees C) and 8/11 (room temperature) fluids. No change in crystal morphology was detected and, apart from one fluid kept at room temperature in which fungal hyphae were noted at six weeks, no new crystals were seen. Calcium pyrophosphate dihydrate crystals in synovial fluid can be maintained for prolonged periods by freezing.

Calcium Pyrophosphate↗
PubMed2004

The ANKH gene and familial calcium pyrophosphate dihydrate deposition disease.

Familial calcium pyrophosphate dihydrate deposition (CPPD) disease is a chronic condition in which CPPD microcrystals deposit in the joint fluid, cartilage, and periarticular tissues. Two forms of familial CPPD disease have been identified: CCAL1 and CCAL2. The CCAL1 locus is located on the long arm of chromosome 8 and is associated with CPPD and severe osteoarthritis. The CCAL2 locus has been mapped to the short arm of chromosome 5 and identified in families from the Alsace region of France and the United Kingdom. The ANKH protein is involved in pyrophosphate metabolism and, more specifically, in pyrophosphate transport from the intracellular to the extracellular compartment. Numerous ANKH gene mutations cause familial CCAL2; they enhance ANKH protein activity, thereby elevating extracellular pyrophosphate levels and promoting the formation of pyrophosphate crystals, which produce the manifestations of the disease. Recent studies show that growth factors and cytokines can modify the expression of the normal ANKH protein. These results suggest a role for ANKH in sporadic CPPD disease and in CPPD associated with degenerative disease.

Animals↗
PubMed2003

Calcium pyrophosphate dihydrate crystal deposition disease.

Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease is characterized by the accumulation of pyrophosphate dihydrate crystals in articular and periarticular tissues. Various terms have been utilized to describe this arthropathy, which has led to some confusion. CPPD crystal deposition disease is among many conditions that may result in crystal deposition within cartilage. Chondrocalcinosis is a pathologic and radiographic term denoting calcification of cartilage within joints including both hyaline articular cartilage and fibrocartilage. Pseudogout is a clinical term applied to an acute inflammatory process in a joint(s) mimicking a gout attack. Pseudogout is just one of the multiple clinical presentations for CPPD crystal deposition disease. Pyrophosphate arthropathy is a term that has been used to describe the peculiar pattern of joint destruction associated with CPPD crystal deposition disease. This article reviews the protean manifestations of CPPD crystal deposition disease with emphasis on diagnostic imaging.

Arthrography↗
PubMed1992

Calcium pyrophosphate crystal deposition disease and other crystal deposition diseases.

A number of cells, chemotactic factors, and inflammatory mediators are implicated in the complex mechanisms underlying crystal-mediated inflammation. Interleukin-8, released from mononuclear cells that have been exposed to urate and other crystals, is a potent chemotaxin and activator of neutrophils. Experimental and clinical observations suggest that joint movements, local biomechanical factors, and previous joint damage may play a role in influencing the intensity of microcrystalline synovitis and the distribution of articular and periarticular crystal deposits in both calcium pyrophosphate dihydrate crystal deposition disease and gout. There are rare reports of extra-articular calcium pyrophosphate dihydrate crystal deposition in tendons, bursae, dura mater, and ligamentum flavum (with radiculomyelopathy) and of massive "tumoral," tophuslike, periarticular calcium pyrophosphate dihydrate crystal deposits. Synovial fluid levels of ATP, the main substrate for nucleoside triphosphate pyrophosphohydrolase ectoenzyme, which cleaves ATP-releasing inorganic pyrophosphate, are higher in patients with calcium pyrophosphate dihydrate crystal deposition disease than in those with other arthritides, and the levels correlate with inorganic pyrophosphate concentrations. Further reports of acute calcific periarthritis of the first metatarsophalangeal joint (hydroxyapatite pseudopodagra) in young women have been described. The mitogenic response of fibroblasts to stimulation with basic calcium phosphate crystals is accompanied by induction and secretion of collagenase and neutral proteases, implicating a role for the crystals in the pathogenesis of both synovial proliferation and joint damage in chronic basic calcium phosphate crystal-associated arthropathy. Subcutaneous cholesterol crystal deposition with tophus formation is extremely rare and has been described in a patient with scleroderma and calcinosis cutis.

Arthritis↗
PubMed1996

Cervical myelopathy caused by calcium pyrophosphate dihydrate crystal deposition in facet joints. A case report.

STUDY DESIGN: This report illustrates a case of cervical myelopathy caused by degenerative changes of the facet joints in which calcium pyrophosphate dihydrate crystals were found histologically. OBJECTIVES: To evaluate the treatment of this patient, which involved the principles of laminoplasty and posterolateral fusion, and to analyze surgical specimens and preoperative radiographs taken after the patient's surgery. SUMMARY OF BACKGROUND DATA: Calcium pyrophosphate dihydrate deposition occurs in cartilage, ligaments, tendons, and joint capsules. Radiographic changes of the cervical facet joints caused by such deposition have already been reported in cadaveric studies. Cases with neurologic compromise rarely occur. METHODS: Surgical specimens that were obtained from the cervical facet joints, i.e., capsule and synovium, were analyzed histopathologically. RESULTS: The preoperative radiographic study showed severe degenerative changes of the cervical facet joints, and analysis of the surgical specimens indicated the presence of calcium pyrophosphate dihydrate crystals. CONCLUSIONS: The cervical facet joints can be involved in calcium pyrophosphate dihydrate crystal deposition and this involvement may accelerate the degenerative changes of the facet joints.

Adult↗
PubMed2001

Foramen magnum syndrome secondary to calcium pyrophosphate crystal deposition in the transverse ligament of the atlas.

STUDY DESIGN: This report illustrates two rare cases of foramen magnum syndrome caused by a retro-odontoid mass in which calcium pyrophosphate dihydrate crystals were found. OBJECTIVES: To analyze the preoperative studies and the diagnostic criteria and to discuss the surgical treatment. The present cases will be compared with previous ones described in the literature. SUMMARY OF BACKGROUND DATA: Deposition of calcium pyrophosphate dihydrate crystals occurs into the fibrous and hyaline cartilage of the joints and intervertebral discs of the spine. Half of the patients known to have a chondrocalcinosis had asymptomatic calcification in the odontoid region. Ten patients were published in the literature as having a spinal cord syndrome secondary to calcium pyrophosphate dihydrate deposition in the odontoid region. METHODS: In both cases the preoperative studies were analyzed, and the retro-odontoid mass was resected and histologically examined. Both had an anterior transoral approach and have been followed for 1 year. RESULTS: According to the preoperative radiographs the diagnosis was suspected and confirmed histologically. Transoral approach was done with no need in either case for a posterior stabilization. CONCLUSIONS: Compression of the spinal cord by calcium pyrophosphate dihydrate deposition may occur. The preoperative diagnosis may be highly suspected after radiographic study and histologically confirmed. Transoral resection is the treatment of choice. Posterior stabilization should be considered only in cases of craniovertebral instability.

Aged↗
PubMed2000

Induction of an acute attack of calcium pyrophosphate dihydrate arthritis by intra-articular injection of hylan G-F 20 (Synvisc).

Little is known about the induction of acute calcium pyrophosphate dihydrate arthritis after the intra-articular injection of hylan G-F 20 (Synvisc). Two reports have documented this adverse effect after the intra-articular injection of hyaluronan. Our patient, a 60-year-old man with osteoarthritis in both knees, presented with a history of an arthroscopy with meniscus shaving 7 years previously. He was given an injection of hylan G-F 20 in the right knee joint. Two days after the second injection, pain and swelling of the knee occurred. There was a severe loss of physical function. Systemic inflammatory reactions such as fever were not observed. A microscopic investigation of the synovial fluid showed evidence of calcium pyrophosphate dihydrate crystals. Bacterial contamination was not detected. There was no indication for calcium pyrophosphate dihydrate in the history of the patient. Some days after receiving nonsteroidal anti-inflammatory drugs and an intra-articular injection of steroids, the symptoms disappeared.

Acute Disease↗
PubMed2000

Formation of calcium pyrophosphate crystals: biologic implications.

The formation of calcium pyrophosphate dihydrate (CPPD) crystals in articular cartilage marks the earliest known phase of CPPD deposition disease. Although the exact mechanisms through which these crystals form remains unknown, work over the last year has added useful details to our current paradigms of crystal nucleation and growth. Key advances include (1) progress in understanding pyrophosphate elaboration and its modifiers, (2) further characterization of the enzymes responsible for pyrophosphate elaboration, and (3) the discovery of an association between two seemingly unrelated metabolic risk factors for CPPD deposition disease.

Arthritis, Rheumatoid↗
PubMed2004

Differential effect of calcium phosphate and calcium pyrophosphate on binding of matrix metalloproteinases to fibrin: comparison to a fibrin-binding protease from inflammatory joint fluids.

The ability of calcium phosphate (CaP) and calcium pyrophosphate (CaPPi) to mediate matrix metalloproteinase-2 and -9 (MMP-2 and MMP-9) binding to fibrin was evaluated. Substrate gel electrophoresis (gelatin zymography) revealed that CaP bound MMP-2 and MMP-9, forming a high molecular weight aggregate with lowered electrophoretic mobility. Formation of the CaP : MMP aggregate was necessary for fibrin binding. In contrast, CaPPi did not aggregate MMPs and did not promote uptake of MMPs into fibrin. Scatchard analysis (Ca/P ratio) revealed that CaPPi (1.96) was chemically similar to calcium pyrophosphate dihydrate (2.00) compared to amorphous CaP (1.50) or crystalline CaP, hydroxyapatite (1.66). MMP : CaP interaction appeared to be electrostatic in nature as high salt concentration (NaCl > 150 mm) reduced binding. In contrast, two non-ionic detergents (Brij-35 and Tween-20) did not prevent MMP : CaP binding. MMP : CaP interaction did not involve the C-terminal MMP region because the specific tissue inhibitor of metalloproteinases (TIMPs) also did not block MMP : CaP interaction and fibrin binding. Although MMP : CaP binding could be decreased with albumin, this effect appeared non-specific due to the high albumin concentration required. High albumin concentration could also partially dissociate preformed MMP : CaP complexes. Interestingly, type I and type IV collagen substantially increased MMP : fibrin-binding activity, whereas denatured collagen, gelatin, did not. Inflammatory joint fluid from five patients also demonstrated similar MMP fibrin-binding activity consistent with CaP mediation. The relevance of these findings to CaP and CaPPi in the pathogenesis of crystal arthropathies such as basic calcium phosphate (BCP) and calcium pyrophosphate dihydrate crystal disease (CPPD) is discussed.

Adult↗
PubMed1971

Differential membranolytic effects of microcrystalline sodium urate and calcium pyrophosphate dihydrate.

Microcrystals of sodium urate produced direct lysis of erythrocyte membranes, as had been described previously for silica. Calcium pyrophosphate crystals induced modest erythrocyte hemolysis, also, and time-course experiments showed a markedly different reaction curve from those produced by silica and urate. Polyvinylpyridine-N-oxide, a strong hydrogen acceptor, was bound from solution to urate and silica, but not to calcium pyrophosphate crystals; this compound effectively blocked urate and silica, but not calcium pyrophosphate or control hemolysis. Dextran and heparin inhibited urate-but not silica-induced hemolysis. If erythrocyte and lysosome membranes react similarly to these particles, then the absence of phagosomes in gouty synovial fluid leukocytes, and the presence of these structures in pseudogout, may be explained.

Cell Membrane↗
PubMed1985

[Crystalline calcium pyrophosphate dehydrate deposit disease].

Radiographic features of calcium pyrophosphate dihydrate (CPPD) crystal deposition disease are outlined in an investigation of 32 patients, with definite or probable disease (according to the diagnostic criteria previously utilized by McCarty). The crystal deposits within fibro- and hyaline cartilage (chondrocalcinosis) may produce an acute synovitis (pseudogout syndrome), and in some patients a radiographically distinctive degenerative arthropathy (pyrophosphate arthropathy). These abnormalities are most frequent in the knee, wrist and symphysis pubis, but often other joints may be affected. Although the alterations superficially resemble osteoarthritis, they are more severe and progressive (Charcot-like joint).

Aged↗
PubMed1981

Further observations on the arthropathy of calcium pyrophosphate crystal deposition disease.

The arthropathy of calcium pyrophosphate dihydrate (CPPD) crystal deposition disease is distinctive and may affect lumbar spinal and sacroiliac joints, as well as appendicular joints. Subchondral pseudocysts that are a hallmark of the disease have a variable appearance, but often occur as a typical cluster of subchondral, coalescent lucencies with smudged, sclerotic margins. Structural joint collapse with fragmentation of cartilage and bone may occur and appear to be related, at least in some cases, to antecedent pseudocysts. Characteristic intra-articular osteochondral bodies are often extensive and may affect multiple joints; their pathogenesis is discussed. Articular synovial calcification is common and may be due to calcium hydroxyapatite, as well as CPPD, particularly if advanced degenerative changes are present. Recognition of the radiologic features may be encountered in CPPD crystal deposition disease is important for differential diagnosis.

Aged↗
PubMed1987

Chondrocalcinosis of the temporomandibular joint. Calcium pyrophosphate dihydrate deposition disease.

A case of calcium pyrophosphate dihydrate (CPPD) arthropathy of the temporomandibular joint, seen in a 54-year-old woman, is reported. The patient presented an eight-year history of diffuse swelling with tenderness over the right preauricular region. Surgical exploration of the right temporomandibular joint disclosed calcified masses that were identified as CPPD crystalline materials by histologic and infrared spectrophotometric studies. The occurrence of CPPD arthropathy of the temporomandibular joint is very rare, and this is only the fourth report of such a case, to our knowledge.

Calcium Pyrophosphate↗
PubMed1999

Familial and clinical aspects of calcium pyrophosphate deposition disease.

The mechanisms involved in calcium pyrophosphate dehydrated deposition disease (CPPDD) are unknown and those families with the disease, described in different countries, provide a fertile file for genomic research. Genomic DNA studies in these kindred with secondary or primary form of CPPDD provide a shortcut for trying to investigate the biomolecular basis of the disease. Mutations in the COL2A1 gene have been identified in one family with spondyloepiphyseal dysplasia and secondary deposits of pyrophosphate and apatite crystalline deposits. In another kindred with CPPDD due to precocious osteoarthritis, the phenotype was linked to markers of chromosome 8p. In four other kindreds (British, Argentinean, French, and the United States), the phenotypes were linked to a precise region of chromosome 5p. Two possible genes located in this region that are expressed in the articular cartilage, but of unknown articular physiologic role are being investigated as possible CPPDD genes. From the clinical point of view, CPPDD spectrum of clinical and radiographic manifestations is enlarging, especially those related to spine involvement or pseudo tumoral forms. At the end, the present review of a current therapeutic approach for CPPDD is discussed.

Acute Disease↗
PubMed1998

Calcium pyrophosphate dihydrate deposition in degenerate lumbar discs.

Calcium pyrophosphate dihydrate (CPPD) crystal deposition in lumbar intervertebral discs has been described, but its clinical significance remains unclear. The present study analyzed histological sections of lumbar discs that were obtained from patients undergoing anterior lumbar interbody fusion. Immunohistological staining was undertaken to identify neural elements and blood vessels. Patients with CPPD deposition were compared with a group without CPPD deposition undergoing the same operation. CPPD was found in 15.7% of investigated patients (12.6% of analyzed discs). Deposits were found in areas of the annulus and nucleus showing advanced degeneration. Two patterns were identified: one comprised sharply demarcated rounded deposits, while the other showed diffuse deposition of crystals. There was no association with ingrowth of vascular or neural tissue. Clinical data did not differ significantly in the two groups of patients. However, in all patients with CPPD deposition there was a history of trauma, previous surgery, or both. Isolated CPPD deposition in lumbar intervertebral discs appears to be an incidental finding that is not related to systemic diseases or general arthropathies.

Adult↗
PubMedDate not supplied

Acute sacroiliitis as a manifestation of calcium pyrophosphate dihydrate crystal deposition disease. A report of two cases.

Whereas radiographic lesions of the sacroiliac joints are common in patients with calcium pyrophosphate deposition crystal disease, they are rarely accompanied with clinical symptoms. We report two cases of acute sacroiliitis probably due to calcium pyrophosphate dihydrate deposition disease. The patients were a 53-year-old man and an 82-year-old woman with chondrocalcinosis in other joints and presence on computed tomography studies of the sacroiliac joints of sclerosis and irregularities of the joint margins with a thin linear calcific deposit within the joint. Both patients recovered fully under therapy with colchicine, analgesics and rest. These two cases suggest that acute sacroiliitis can be caused by calcium pyrophosphate dihydrate crystal deposition disease.

Acute Disease↗
PubMed2001

Transforming growth factor beta-1 stimulates articular chondrocyte elaboration of matrix vesicles capable of greater calcium pyrophosphate precipitation.

Objective To determine the role of transforming growth factor beta1 (TGFbeta) in early calcium pyrophosphate formation by measuring its effects on articular chondrocyte matrix vesicle (MV) formation, specific activity of the inorganic pyrophosphate(PPi)-generating enzyme nucleoside triphosphate pyrophospho-hydrolase (NTPPPH) and biomineralization capacity. Methods MV elaborated from mature porcine chondrocyte monolayers+/-TGFbeta were compared for protein content, NTPPPH activity, and ATP-dependent biomineralization. Precipitation of calcium pyrophosphate mineral phases by MV was determined by a radiometric assay and by Fourier transform infrared spectroscopy (FTIR). Results MV from monolayers exposed to TGFbeta were enriched in NTPPPH activity compared to MV from control monolayers (P< 0.01) and precipitated more calcium/mg MV protein than controls (P</= 0.01). FTIR spectra of mineral generated by monolayer-elaborated MV were consistent with poorly crystalline CPPD. Conclusions TGFbeta is capable of increasing the capacity of articular chondrocyte-derived MV to generate PPi via NTPPPH and precipitate calcium in the form of CPPD mineral. These data support the concept that this growth factor plays a key role in cartilage matrix CPPD deposition.

Animals↗