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PubMed1989

Calcium pyrophosphate and monosodium urate crystal interactions with neutrophils: effect of crystal size and lipoprotein binding to crystals.

"Small" (between 75-98% of crystals less than or equal to 10 microns) and "large" (between 81-93% of crystals greater than 10 microns) size fractions of monosodium urate monohydrate (MSUM) and calcium pyrophosphate dihydrate triclinic (CPPD) crystals were incubated with human neutrophils and crystal induced neutrophil cytolysis monitored by measuring the release of lactate dehydrogenase. "Small" size fractions of MSUM and CPPD gave higher percent lysis values than "large" crystals. The binding of high density lipoproteins (HDL) and low density lipoproteins (LDL) to the crystals was quantitated. HDL and LDL bound in significant amounts to both CPPD and MSUM and strongly inhibited CPPD and MSUM induced neutrophil cytolysis. We propose that HDL and LDL bound to MSUM and CPPD may play important roles in the regulation of gouty inflammation.

Apolipoproteins↗
PubMed1994

Pelvic pseudotumoral calcium pyrophosphate dihydrate deposition: an ultrastructural study.

We analyzed large periarticular calcifications of the hips and pubis in a woman with diffuse primary chondrocalcinosis, symptomatic in the knees. Serial articular and periarticular biopsies were obtained during surgery for osteoporotic hip fracture. Histologic examination showed diffuse nonbirefringent clumps in red alizarin stained cartilage, capsula and tendon. Scanning electron microscopy with microanalysis indicated a calcium/phosphorus atomic ratio of about 1. Transmission electron microscopy, electron diffraction and Raman spectroscopy assessed calcium pyrophosphate dihydrate (CPPD) in cartilage, synovia, capsula, tendon and muscle. The cause of these hard to observe, bulky CPPD periarticular deposits, which resembled basic calcium phosphate on radiography, is still unclear.

Aged↗
PubMed1992

Coffin-Lowry syndrome associated with calcium pyrophosphate crystal deposition in the ligamenta flava.

Clinical and ultrastructural study of four cases of Coffin-Lowry syndrome (CLS), a heritable disorder with peculiar facies, stooped posture, vertebral changes, and mental retardation, is reported. Three of the four cases had myelopathy caused by calcification of the ligamenta flava in early adulthood. These patients demonstrated that CLS is a calcium pyrophosphate dihydrate crystal deposition disease, and it is postulated that a metabolic abnormality in collagen and in proteoglycans are responsible for some aspects of CLS.

Adolescent↗
PubMed2003

[Cervical myelopathy induced by calcium pyrophosphate tophus in primary chondrocalcinosis].

A 78 year old female patient with cervical myelopathy induced by a calcium pyrophosphate dihydrate tophus around the dens axis with clinical signs of a cervical tumor is presented. After operation of the tumor, the diagnosis of a generalized CPPD disease was established retrospectively, where by patient had complained of joint pain already for many years. This known complication of a primary chondrocalcinosis should be a reason for a careful investigation of the cervical spine in CPPD disease, because neurological disturbances might increase the joint destruction in the manner of "Charcot joints".

Aged↗
PubMed1985

Histological study of a case of recurrent olecranon bursitis with mixed calcium pyrophosphate dihydrate and apatite crystal deposits.

This is the report of a light and transmission electron microscopic study of an olecranon bursitis and of the adjacent distal tricipital tendon in an 83 year-old man. The data are compared with those of a similar study in the same patient performed 2 years ago. Calcium pyrophosphate dihydrate crystals were observed in the bursal fluid, in the inner part of the bursal wall (extracellular localization and intracellular phagocytosis) as well as in the peripheral part of the tendon. In addition, small apatite deposits were observed in the bursa and tendon by electron microscopy. The origin of these bursal deposits is discussed; it is suggested that they may be related to an exchange from the tendon to the remodelled bursal wall.

Aged↗
PubMed2000

The inhibition of spontaneous and tumor necrosis factor-alpha induced neutrophil apoptosis by crystals of calcium pyrophosphate dihydrate and monosodium urate monohydrate.

OBJECTIVE: Spontaneous neutrophil apoptosis may be inhibited by various proinflammatory stimuli. which may result in prolonged lifetimes and responses of these phagocytic cells with the potential for extended inflammation. We investigated the effect of short term incubation of opsonized crystals of monosodium urate monohydrate (MSUM) or calcium pyrophosphate dihydrate (CPPD) on both spontaneous and tumor necrosis factor-alpha (TNF-alpha) induced neutrophil apoptosis. METHODS: Peripheral neutrophils were incubated with plasma opsonized crystals of CPPD or MSUM in the presence or absence of TNF-alpha for 4 h at 37 degrees C. Apoptosis was determined using 3 separate assays: (1) an agarose DNA fragmentation assay, (2) a cytoplasmic histone associated DNA fragmentation assay, and (3) a caspase 3 fluorometric assay. RESULTS: All 3 assays showed similar results. Both MSUM and CPPD crystals inhibited spontaneous apoptosis in neutrophils. TNF-alpha induced high levels of apoptosis in neutrophils. However, co-incubation of the cells with TNF-alpha and crystals resulted in the inhibition of apoptosis to levels below those of control cells. Pretreatment of neutrophils with the protein synthesis inhibitor cycloheximide prevented the inhibition of apoptosis by crystals. CONCLUSION: These data support the concept of crystal induced inhibition of neutrophil apoptosis as part of the pathophysiology of the diseases collectively known as crystal induced arthritis.

Apoptosis↗
PubMed2004

Calcium pyrophosphate dihydrate crystal associated induction of neutrophil activation and repression of TNF-alpha-induced apoptosis is mediated by the p38 MAP kinase.

The role of p38 mitogen-activated protein (MAP) kinase in the activation of human neutrophils and repression of TNF-alpha-induced apoptosis in response to plasma opsonized crystals of calcium pyrophosphate dihydrate (CPPD) was investigated. We monitored the endogenous phosphotransferase activity of p38 kinase in neutrophils stimulated with CPPD crystals (25 mg/ml) alone or in the presence of TNF-alpha (10 ng/ml), and with TNF-alpha alone. CPPD crystals induced a 2-fold activation of p38 kinase activity over the basal activity that was observed in untreated neutrophils. Furthermore, CPPD crystals repressed the TNF-alpha associated 6-fold induction of p38 kinase phosphotransferase activity to levels associated with CPPD crystal incubation alone in a PD98059 (20 ng/ml) and Wortmannin (100 nM) sensitive manner. Inhibition of CPPD crystal-induced activation of the neutrophil inflammatory response as measured by chemiluminescence, superoxide anion generation and degranulation as determined by myeloperoxidase and lysozyme release was observed in the presence of the specific p38 MAP kinase inhibitor SB203580 (5 microM). CPPD crystal associated repression of TNF-alpha-induced activation of neutrophil apoptosis as determined by DNA fragmentation correlated with the CPPD crystal mediated inhibition of p38 kinase activity, probably through crystal inhibition of caspase 3. Together, our results indicate that the CPPD crystal associated inflammatory response is regulated through the activation of p38 kinase to sub-apoptotic levels, and that the repression of the TNF-alpha-induced apoptosis program in neutrophils is mediated via the repression of caspase 3 mediated apoptosis-associated p38 kinase activity.

Androstadienes↗
PubMed1999

Selective inhibition of protein kinase C, mitogen-activated protein kinase, and neutrophil activation in response to calcium pyrophosphate dihydrate crystals, formyl-methionyl-leucyl-phenylalanine, and phorbol ester by O-(chloroacetyl-carbamoyl) fumagillol (AGM-1470; TNP-470).

The effect of O-(chloroacetyl-carbamoyl) fumagillol (AGM-1470; TNP-470) was investigated on protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) activation in neutrophils stimulated by plasma-opsonized crystals of calcium pyrophosphate dihydrate (triclinic) [CPPD(T)], formyl-Met-Leu-Phe (fMLP), and phorbol 12-myristate 13-acetate (PMA). Neutrophil respiratory burst responses also were determined in AGM-1470-pretreated cells stimulated with the same agonists, using chemiluminescence and superoxide anion generation assays. AGM-1470 (5 microM) effectively inhibited PKC activation in cells treated with CPPD(T) crystals (50 mg/mL, 2 min) and fMLP (1 microM, 1 min), but had no effect on PMA-treated cells (0.5 microM, 5 min). AGM-1470 blocked MAPK activity completely and reduced neutrophil activation induced by fMLP and PMA but not by CPPD(T). The degree of inhibition of the respiratory burst plateaued at approximately 46+/-9 and 54+/-3% in fMLP- and PMA-treated cells, respectively. These data indicate that activation of neutrophil respiratory burst activity may be mediated through the MAPK pathway. AGM-1470 pretreatment did not inhibit CPPD(T) crystal- or fMLP-stimulated phosphatidylinositol 3-kinase (PI 3-kinase) activity. These findings, coupled with further observations that the PI 3-kinase inhibitor wortmannin (10 nM) inhibited fMLP- and CPPD(T) crystal-induced but not PMA-induced chemiluminescence, indicate that at least two distinct signaling pathways (mediated by PI 3-kinase or MAPK) lead to neutrophil respiratory burst responses. PKC may also be required in the MAPK-stimulated pathway. We propose that the inhibitory effect of AGM-1470 on the neutrophil respiratory burst may be due to its ability to inhibit PKC and MAPK activation.

Calcium Pyrophosphate↗
PubMed1975

An ultrastructural study of the articular cartilage in calcium pyrophosphate dihydrate (CPPD) crystal deposition disease (chondrocalcinosis articularis).

An ultrastructural study of articular cartilage from five patients with calcium pyrophosphate dihydrate (CPPD) crystal deposition disease was performed. The CPPD crystals, identified by micro X-ray diffraction, were usually found in clusters, located in intercellular areas of the intermediate cartilage layer. The matrix surrounding the clusters either showed a normal morphology or a homogeneous appearance, within which faint cross striations but no distinctly fibrillar outlines could be identified. Another change in the matrix, characterized by an increased electron density and longitudinally fragmented collagen fibres, was also seen. This latter change was generally seen without concomitant CPPD crystal deposition. No specific relationship between the crystals and the collagen fibres or the granular background material of the matrix was encountered.

Adult↗
PubMed2001

Inhibitory effect of low density lipoprotein on the inflammation-inducing activity of calcium pyrophosphate dihydrate crystals.

OBJECTIVE: It has been proposed that low density lipoprotein (LDL) plays a role in the self-limiting nature of pseudogout inflammation. We investigated changes of LDL concentration in rat air pouch fluid during periods of acute and subsiding inflammation to evaluate whether LDL contributes to inhibiting inflammation of pseudogout. We examined whether LDL binds to calcium pyrophosphate dihydrate (CPPD) crystals as a possible mechanism for reduction of inflammation. METHODS: In this in vivo study, 5 mg suspensions of CPPD crystals and saline were injected into the rat air pouch. Fluid samples were taken from rat air pouch at 0, 3, 6, 12, 24, and 48 h after injection. White blood cells in the samples were counted; the remaining fluid was centrifuged and concentrations of beta-glucuronidase and PGE2 in the supernatant were measured as inflammatory markers. LDL in the supernatant was immunochemically identified by Western blotting, then pellets containing crystals were examined by the same technique. RESULTS: LDL was identified in the air pouch 3 h after CPPD crystal injection, and its concentration increased and reached a peak level after 24 h. Inflammatory markers reached maximal level from 6 to 12 h, then decreased after 24 h. In the pellets containing crystals, LDL could not be identified in every specimen. CONCLUSION: LDL in the rat air pouch increased during the inflammatory course induced by CPPD crystal and the inflammation subsided as the LDL increased. Since some reports indicate LDL was related to reduction of crystal induced inflammation such as gout or pseudogout, we concluded that LDL could contribute to the resolution of acute pseudogout arthritis in vivo with or without binding to CPPD crystals.

Animals↗
PubMed1994

Characterization of chondrocyte alkaline phosphatase as a potential mediator in the dissolution of calcium pyrophosphate dihydrate crystals.

OBJECTIVE: To characterize chondrocyte alkaline phosphatase (ALP) distribution and expression in cartilage and monolayer cultures. METHODS: Sections of bovine articular cartilage or chondrocyte monolayer cultures were stained for ALP activity. Surface ALP was released with bacterial phosphatidylinositol specific phospholipase C (PI-PLC). The levels of ALP mRNA were determined by Northern blot analysis using a cDNA probe to bovine ALP. RESULTS: Chondrocyte ALP activity dissolves calcium pyrophosphate dihydrate (CPPD) crystals. About 5% of the total chondrocytes contained ALP activity. The ALP positive cells were present only in the deep layers of articular cartilage adjacent to the subchondral bone. Thirty to forty percent of the total ALP activity was present on the chondrocyte surface and was released by PI-PLC. Both chondrocyte ALP activity and mRNA levels decreased with time in culture. However, continuous dexamethasone treatment stimulated the expression of ALP in ALP positive chondrocytes, sufficiently to replace all of the chondrocyte surface ALP released following PI-PLC treatment. CONCLUSION: Since ALP hydrolyzes pyrophosphate and dissolves CPPD crystals, our data suggest that regulation of chondrocyte ALP activity and expression in cartilage may prove useful for the development of a specific therapy CPPD arthropathy.

Alkaline Phosphatase↗
PubMed1996

Cubital tunnel syndrome associated with calcium pyrophosphate dihydrate crystal deposition disease.

Nine patients (11 elbows) presented with cubital tunnel syndrome that was complicated by calcium pyrophosphate dihydrate (CPPD) crystal deposition disease. Their age ranged from 63 to 86 years, and 8 of the 9 patients were more than 70 years old. X-ray film examination demonstrated the presence of CPPD crystal deposition not only in the elbow but also in the knee, wrist, or spine in all patients. Medial epicondylectomy was performed in 8 patients (9 elbows), while 1 patient with both elbows affected was treated conservatively at his request. Thickening of the ulnar collateral ligament and synovium due to CPPD crystal deposition and degenerative joint changes induced protrusion of the floor of the cubital tunnel, resulting in ulnar neuropathy in these patients. The ulnar nerve was compressed between the protruded floor and fibrous band. Though various causes of cubital tunnel syndrome have been reported, findings of this study indicate that CPPD crystal deposition disease should also be considered a cause of this syndrome.

Aged↗
PubMed1995

Distribution of calcification in the triangular fibrocartilage region in 181 patients with calcium pyrophosphate dihydrate crystal deposition disease.

PURPOSE: To investigate the occurrence of calcification around the triangular fibrocartilage complex in calcium pyrophosphate dihydrate (CPPD) crystal deposition disease. MATERIALS AND METHODS: The radiographs of 316 wrists in 181 patients with a definite or probable diagnosis of CPPD disease were reviewed to determine the occurrence of calcification in the inferior radioulnar joint cartilage, triangular fibrocartilage, lunotriquetral ligament, lunotriquetral cartilage, and triquetral cartilage. RESULTS: The distribution of calcification in the 316 wrists was as follows: inferior radioulnar joint cartilage, 87 wrists (28%), triangular fibrocartilage, 233 (74%); lunotriquetral ligament, 244 (77%); lunotriquetral cartilage, 167 (53%); and triquetral cartilage, 66 (21%). Forty-nine wrists had calcification in the lunotriquetral ligament or cartilage but not in the triangular fibrocartilage; 30 wrists had calcification in the triangular fibrocartilage but not in the lunotriquetral ligament or cartilage. This difference in prevalence was statistically significant (P = .0429). CONCLUSION: Radiologic diagnosis of CPPD crystal deposition disease in the wrist necessitates careful evaluation of the lunotriquetral ligament as well as the triangular fibrocartilage.

Aged↗
PubMedDate not supplied

Acute sacroiliitis as a manifestation of calcium pyrophosphate dihydrate crystal deposition disease.

While radiographic lesions of the sacroiliac joint (SIJ) are common in patients with calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, they are rarely accompanied by clinical symptoms. We report the case of a 69-year-old woman who presented with an acute sacoiliitis and a linear calcification in the right SIJ on CT scan. The patient recovered well after intra-articular steroid injections.

Acute Disease↗
PubMed1984

Mitogenic effects of hydroxyapatite and calcium pyrophosphate dihydrate crystals on cultured mammalian cells.

Synthetic hydroxyapatite (HA) crystals in 1% serum stimulated 3H thymidine uptake into quiescent canine synovial fibroblasts and human foreskin fibroblast cultures, as did 10% serum. The onset of stimulation and peak uptake of thymidine after crystal addition were delayed by 2-3 hours as compared with the effects produced by 10% serum. Stimulation of 3H thymidine uptake was proportional to the serum concentration used. HA crystals (50 micrograms/ml) stimulated nuclide uptake at each serum concentration used. 3H thymidine uptake was also proportional to the dose of HA or calcium pyrophosphate dihydrate crystals, although larger doses of the latter crystal were required to produce equivalent effects. Not all particulates were effective mitogenic agents. Latex beads and diamond crystals had no effect. Monosodium urate crystals modestly stimulated and calcium urate crystals markedly stimulated nuclide uptake. The more complex crystals found in a naturally occurring condition (calcinosis) were as mitogenic as the pure synthetic HA. The synovial cell hyperplasia sometimes associated with crystals might be explained in part by their mitogenic activity.

Animals↗
PubMed2005

Calcium pyrophosphate dihydrate crystal deposition disease of the temporomandibular joint.

A case of a 74-year-old woman with calcium pyrophosphate dihydrate crystal deposition disease of the temporomandibular joint (TMJ) is presented. This disease rarely involves the TMJ and is not usually considered in the differential diagnosis of TMJ disorders. To our knowledge, only 23 cases have been reported in the literature and only four without any destructive changes of the condyle as in the present case.

Aged↗
PubMed1982

Enzymatic release of microspheroids containing hydroxyapatite crystals from synovium and of calcium pyrophosphate dihydrate crystals from cartilage.

Incubation of minced, focally calcified, chondromatosis tissue obtained at operation from a patient with Milwaukee shoulder (rotator cuff defect and glenohumeral osteoarthritis associated with synovial fluid, hydroxyapatite crystals in microspheroidal masses, collagenase, and neutral protease) with partially purified mammalian synovial cell collagenase released masses of hydroxyapatite crystals of the same size as those originally found in the patient's synovial fluid. Incubation of mineral articular cartilage obtained from a shoulder joint at arthroplasty for a destructive arthropathy in a patient with generalised calcium pyrophosphate dihydrate (CPPD) crystal deposition with partially purified synovial cell collagenase freed CPPD crystals from their matrix. These data are compatible with a previously postulated mechanism linking microcrystals to destructive arthropathies, that is, crystal endocytosis by synovial cells stimulating collagenase secretion with subsequent enzymatic crystal "strip-mining', releasing additional crystals into the synovial fluid in a self-perpetuating cycle.

Calcium Pyrophosphate↗